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International Vascular Biology Meeting 2018

President

http://jvbmo.umin.jp/

The Office

The Japanese Vascular Biology and Medicine Organization(JVBMO)

Masayuki Yoshida, MD

The JVBMO supports all vascular-researchers in basic and clinical sciences to perform exciting presentations, deep discussions and free communications. The JVBMO is an Asian representative member for International Vascular Biology Meeting(IVBM).

c/o Proactive Inc. 3F Sannomiya Century Bldg, 83 Kyomachi Chuo-ku, Kobe 650-0034, Japan FAX: +81-78-332-2506 E-MAIL： [email protected]

Copyright © 2018 PerkinElmer, Inc. 400318_15 All rights reserved. PerkinElmer® is a registered trademark of PerkinElmer, Inc. All other trademarks are the property of their respective owners.

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Contents

Welcome words ..................................................................................6

Committees .........................................................................................8• OrganizingCommittee .................................................................8• LocalOrganizingCommittee ........................................................8• CongressOffice ............................................................................8• InternationalScientificProgramCommittee ...............................9

CollaboratingSocieties .....................................................................11Sponsors ............................................................................................12Exhibitors ..........................................................................................13ExhibitionGuide ................................................................................14

ProgramataGlance .........................................................................16

Program .............................................................................................17

Abstracts ...........................................................................................28• Monday ......................................................................................28• Tue ..............................................................................................78• Wed ......................................................................................... 126

Authorindex .................................................................................. 172

Speakers ......................................................................................... 200

Participants .................................................................................... 206

Wihuri Research Institute (WRI), supported by the Jenny and Antti Wihuri Foundation, is a non-profit biomedical research institute focused on the cardiovascular system in disease. The mission of the Institute is to achieve new fundamental and translational understanding of the

molecular and cellular basis of the vascular system and its involvement in disease pathogenesis, for the benefit of mankind. Discovery and translational research in the Institute

focuses on vascular and regenerative medicine and growth factor signaling mechanisms, using new technologies such as single-cell sequencing and genomic editing of stem cells.

The Jenny and Antti Wihuri Foundation is a DIAMOND SPONSOR of IVBM2018.

Advancing first-in-class treatments targeting the Tie2 Pathway for ocular diseases and diabetes

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Dear Colleagues, It is a true pleasure to welcome you to Helsinki for the 20th International Vascular Biology meeting (IVBM2018). IVBM2018 continues the important tradition of bringing together the global vascular biology community to share the newest advancements in the field. Our goal is that the IVBM2018 will present the best vascular biology research from all parts of the world, by researchers of all ages and genders, and promote global exchange of ideas between established and young researchers from academia, clinical medicine and pharmaceutical industry. We are thrilled about the fabulous and diverse list of speakers from all over the world at IVBM2018. We hope that IVBM2018 will bring a lasting impact and promote further breakthroughs and paradigm shifts. We are excited to see many interfaces to other disciplines represented – such as interfaces to immunology, neurobiology and metabolism, just to mention few. This multidisciplinary nature of IVBM2018 highlights the relevance of vascular biology to an increasing number of diseases affecting essentially every organ in our bodies. In IVBM2018, you will see and hear many examples of this, and of many new technologies that allow us to dive deeper into organ-specific vascular diversity in structure and function. We are extremely grateful for the collaboration and partnership of the International Scientific Program Committee in launching the conference. We are also thankful for the Local Organizing Committee for their immense efforts, and members of the local Scientific Crew, who, putting their own research aside, have helped greatly in making IVBM2018 possible and continue serving participants during the meeting. We are tremendously delighted to have our partner societies from all parts of the globe join us in this event. These include the European Vascular Biology Organization, the French Angiogenesis Society, the Japanese Vascular Biology and Medicine Organization, the Korean Society for Vascular Biology and Medicine, the North American Vascular Biology Organization and the Lymphatic Education & Research Network. The support for this meeting has been exceptional, and includes support from institutions, societies, foundations, companies, and organizations. We are most grateful for these partnerships and their generous support. Please take the time to visit the IVBM2018 website (www.helsinki.fi/ivbm2018) to appreciate our many supporters. We are, in turn, dedicated to our partnership with the sponsors in order to organize, support, and facilitate a meeting that will inform, inspire, and foster collaboration. We wish to express our gratitude to all participants of IVBM2018. Your participation will make IVBM2018 an outstanding opportunity to promote collaborations and strengthen our research community. We hope you will enjoy these summer days in Helsinki! - Thank you for joining us at IVBM2018! The Organizing Committee:

Kari Alitalo Christer Betsholtz Lena Claesson-Welsh

Jozef Dulak Pipsa Saharinen Seppo Ylä-Herttuala

Lipedema is a chronic condition that symmetrical buildup of painful fat ad swelling in the arms and legs, sparing the hands and feet. It occurs almost exclusively in women and is poorly understood.

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Committees

Local Organizing Committee

Michael Jeltsch,PhDAdjunctProfessor,AcademyResearchFellowUniversityofHelsinki&WihuriResearchInstituteHelsinki,Finland

Sinem Karaman,PhD TeamleaderWihuriResearchInstitute&UniversityofHelsinkiHelsinki,Finland

Riikka Kivelä,PhDAcademyResearchFellow,GroupleaderUniversityofHelsinki&WihuriResearchInstituteHelsinki,Finland

Committees

Kaisa Sarkkinen ProjectCoordinatorUniversityofHelsinkiHelsinki,Finland

Laura FellmanSecretaryWihuriResearchInstituteHelsinki,Finland Congress Organiser

Riikka LouhivuoriCongress&EventsManagerConfedentInternationalHelsinki,Finland

Organizing Committee

Kari Alitalo, M.D.,Ph.D.AcademyProfessor,DirectorofWihuriReserachInstituteUniversityofHelsinki&WihuriResearchInstituteHelsinki,Finland

Jozef Dulak, Ph.D.,D.Sc. Professor,HeadoftheDepartmentJagiellonianUniveristyKrakow,Poland

Christer Betsholtz, D.M.Sc. ProfessorinTumorBiologyKarolinskaInstitutet&UppsalaUniversityUppsala,Sweden

Pipsa Saharinen, PhD PrincipalInvestigatorUniversityofHelsinki&WihuriResearchInstituteHelsinki,Finland

Lena Claesson-Welsh, B.D.,Ph.D. ProfessorinVascularBiologyUppsalaUniversityUppsala,Sweden

Seppo Ylä-Herttuala, M.D.,Ph.D.AcademyProfessor,GroupLeaderUniversityofEasternFinlandKuopio,Finland

International Scientific Program CommitteeCommittees

MarcAchen PeterMaccalllumCancerCentre

RalfAdams MaxPlanckInstituteforMolecularBiomedicine

YvonneAlexander ManchesterMetropolitanUniversity

ZoltanArany UniversityofPennsylvaniaHellmutAugustin HeidelbergUniversity&

GermanCancerResearchCenter

AndreaBanfi BaselUniversityHospitalVictoriaBautch TheUniversityofNorth

Carolina-ChapelHillGabrieleBergers Vib-centerforCancerBiologyAndreasBikfalvi InsermJoyceBischoff BostonChildren’sHospital

andHarvardMedicalSchoolTatianaByzova ClevelandClinicMagnusBäck KarolinskaUniversityHospitalElisabettaDejana FircInstituteofMolecular

OncologyMichaelDellinger UtSouthwesternMedical

CenterMichaelDetmar EthZurichAnnaDimberg UppsalaUniversityAnneEichmann YaleUniversityLauriEklund UniversityofOuluUlfEriksson KarolinskaInstitutetAndreasFischer GermanCancerResearch

CenterHolgerGerhardt Max-Delbrueck-Centerfor

MolecularMedicineStephaneGermain INSERMU1050CeciliaGiachelli UniversityofWashingtonNatashaHarvey UniversityofSouthAustraliaYulongHe SoochowUniversityKarenHirschi YaleUniversityTimothyHla BostonChildrensHospital/

HarvardMedicalSchoolBenHogan UniversityofQueenslandYoung-KwonHong UniversityofSouthern

CaliforniaBeatImhof UniversityofGenevaLuisaIruela-Arispe UCLADavidJackson UniversityofOxfordRakeshJain HarvardMedicalSchoolSirpaJalkanen UniversityofTurkuRandallJohnson UniversityofCambridge/

KarolinskaInstituteMinnaKaikkonen-Määttä

UniversityofEasternFinland

SinemKaraman WihuriResearchInstituteandUniversityofHelsinki

DontschoKerjaschki MedicalUniversityofVienna,Dept.Pathology

EliKeshet HebrewUniversityLevonKhachigian UniversityofNewSouth

Wales,SydneyFriedemannKiefer EuropeanInstitutefor

MolecularImaging,WWUMünster

JanKitajewski UniversityofIllinoisatChicago

RiikkaKivelä UniversityofHelsinkiGouYoungKoh Ibs/KaistPetriKovanen WihuriResearchInstituteFerdinandLeNoble KarlsruheInstituteOf

Technology(kit)XuriLi ZhongshanOphthalmic

CenterDonaldMcDonald UCSFNaokiMochizuki Natl.Cerebr.&Cardiovasc.

Ctr.JapanTaijaMäkinen UppsalaUniversityStefaniaNicoli YaleUniversityVesaOlkkonen MinervaFoundationInstitute

ForMedicalResearchGaryOwens UniversityofVirginiaSchool

ofMedicineSamirParikh HarvardMedicalSchool-beth

IsraelDeaconessTatianaPetrova UniversityOfLausanneMichaelPotente MaxPlanckInstituteforHeart

andLungResearchAnnaRandi ImperialCollegeLondonKristyRed-Horse StanfordUniversityYvonneReiss GoetheUniversityHospital

FrankfurtMartinSchwartz YaleUniversityWilliamSessa YaleUniversityMichaelSimons YaleUniversityJean-LeonThomas InsermDietmarVestweber MaxPlanckInstituteof

MolecularBiomedicineMiikkaVikkula DeDuveInstitute,Universite

CatholiquedeLouvainKennethWalsh BostonUniversitySchoolof

MedicineTetsuroWatabe TokyoMedicalandDental

UniversityJunYamashita CenterForIpsCellResearch

&Application,KyotoUniversity,

Ylä-Herttuala,Seppo A.I.VirtanenInstitute,UniversityOfEasternFinland

BinZhou ChineseAcademyofSciencesÖörni,Katariina WihuriResearchInstitute

Collaborating Societies

SponsorsDiamond Level Sponsors

Platinum Level Sponsor

Gold Level Sponsors

Silver Level Sponsors

Contributors and Partners

Exhibitors

Advertisers: 3Scan, Eatris, KDBIO, Labema Oy, Lipedema

Exhibition Guide

Entrance 1st Floor

Ground Floor

Karamzininranta

Posters & Exhibition

2nd Floor

Mannerheimintie

Lift

Goods lift

Guide display (portrait)

Media display (landscape)

Foyer Level, 2 floornd

Main Building

FINLANDIA HALL-

SOLOIST ROOMS

ORCHESTRA LOUNGE

HELSINKI HALL

FINLANDIA HALL-( )FOYER PIAZZA

VIP FOYER

HELSINKI HALL-FOYER

RESTAURANT1HALL

RESTAURANT2HALL

RESTAURANT3HALL

1 2 3 4 5 10 20m

28.5.2017 Maarit Loimijoki

IVBM 2018Finlandia Hall3.-7.6.2018

Stand 06ibidid Gmbh

Stand 05

Svanholm.com Aps

Stand 04

Caltag

Medsystems

Stand 03

Bioscientifica

Stand 02

Cell Biologics,

Inc.

Stand 01

Bio-rad

Laborarories Ltd

Stand 07PromegaBiotech Ab

Stand 08Perkin ElmerFinlandOy

Stand 09FujifilmVisualsonics

Stand 16Carl Zeiss Oy

Stand 15Pfizer

Stand 14MoorInstruments Ltd

Stand 13Promocell Gmbh/Biotop Oy

Stand 11Janvier Labs

Stand 10Sartorius

A Brief History of Blood and Lymphatic Vessels

By Andreas Bikfalvi2017. XIII, 192, 9 illu. 52 illu in colour. Softcover.€ (D) 96,29 | € (A) 98,99 | *sFr 99,00ISBN 978-3-319-74375-2€ 74,96 | *sFr 79,00ISBN 978-3-319-74376-9 (eBook)

• Most complete history of our understanding of angiogenesis and vascular biology today

• First conceptual and philosophical analysis in the field • In dept discussion of our current understanding of angiogenesis

and vasculature

This book provides a comprehensive account of vascular biology and pathology and its significance for health and disease. It systematically and chronologically explains how we came to our current understanding of the vasculature and it´s function today, and describes in an entertaining way the diverse flaws and turns in science and medicine from the past.

The first € price and the £ and $ price are net prices, subject to local VAT. Prices indicated with * include VAT for books; the €(D) includes 7% for Germany, the €(A) includes 10% for Austria. Prices indicated with ** include VAT for electronic products; 19% for Germany, 20% for Austria. All prices exclusive of carriage charges. Pricesand other details are subject to change without notice. All errors and omissions excepted.

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Program at a Glance

Monday, June 4, 201808:30–09:50 Plenary session II – Finlandia Main Hall09:50–10:15 Coffee Break

Helsinki Hall Veranda 1 Veranda 2 Veranda 310:15–12:15 Parallel session 1:

AtherosclerosisParallel session 2: Blood brain barrier

Parallel session 3: TIE2 pathway in vascular disease

Parallel session 4: Metabolic disease

12:15–12:45 Lunch12:30–13:00 Lunch Seminar12:45–14:15 Poster session I - Finlandia Hall Piazza14:15–16:00 Parallel session 5:

Vascular infl ammationParallel session 6: Mechanotrans-duction & ECM

Parallel session 7: Vessel development & stability

Parallel session 8: Lymphatic specifi cation & morphogenesis

16:00–16:30 Coffee Break16:30–17:50 Plenary session III – Finlandia Main Hall18:30 Reception at Helsinki City Hall

Tuesday, June 5, 201808:30–09:50 Plenary session IV – Finlandia Main Hall09:50–10:15 Coffee Break

Helsinki Hall Veranda 1 Veranda 2 Finlandia Hall10:15–12:15 Parallel session 9:

Neuro-vascular interactions & disease

Parallel session 10: Endothelial cell metabolism & angiogenesis

Parallel session 11: Vascular signalling

Parallel session 12: Targeting tumor vasculature

12:15–12:45 Lunch12:45–14:15 Poster session II - Finlandia Hall Piazza14:15–16:15 Parallel session 13:

Cardiovascular disease

Parallel session 14: Vascular smooth muscle cells

Parallel session 15: Lymphangiogenesis

Parallel session 16: Tumor angiogenesis

16:15–16:45 Coffee Break16:45–18:05 Plenary session V – Finlandia Main Hall

18:10–19:10 Meet the editors

16:30-18:30 ESC round table

18:10–19:10 Showcases

Wednesday, June 6, 201808:30–09:50 Plenary session VI – Finlandia Main Hall09:50–10:15 Coffee Break

Helsinki Hall Veranda 1 Veranda 2 Veranda 310:15–12:15 Parallel session 17:

Leukocyte traffi cking & endothelial barrier function

Parallel session 18: Novel functions of lymphatic vessels

Parallel session 19: Angiogenesis

Parallel session 20: Mechanisms of vascular disease

12:15–12:45 Lunch12:45–14:15 Poster session III - Finlandia Hall Piazza14:15–16:00 Parallel session 21:

Organotypic vasculature

Parallel session 22: Endothelial regeneration & senescence

Parallel session 23: Vascular physiology & pathology

Parallel session 24: Epigenetics & genetics of vascular differentiation

16:00–16:30 Coffee Break

16:30–18:50 Plenary session VII & Workshop on Vascular Single-Cell RNA Sequencing – Finlandia Main Hall

19:00 Nordic Night at Allas Sea Pool

Thursday, June 7, 2018 Helsinki Hall Veranda 1 Veranda 2 Veranda 3

08:30–09:30 Parallel session 25: Vascular anomalies

Parallel session 26: Clinical translation

Parallel session 27: Arteriogenesis

Parallel session 28: Fluid shear stress regulation

09:30–10:00 Coffee Break10:00–12:30 Plenary session VIII & Poster/Travel award & Closing remarks - Finlandia Main Hall

– 17 –

IVBM2018Program

Sunday, June 3, 2018

17:00-19:30 Plenary session ICo-sponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Finlandia Main HallChairs: Lena Claesson-Welsh, Pipsa Saharinen, Christer Betsholtz & Kari Alitalo17:30-18:10 Napoleone Ferrara (San Diego, CA, USA) Current state of anti-angiogenic therapies18:10-18:50 Susan Quaggin (Chicago, IL, USA) Stolen identities - new vascular phenotypes Tie’d to disease18:50-19:30 Helen Hobbs (Dallas, TX, USA) ANGPTLs, lipid metabolism and energy homeostasis

19:30 Welcome Reception at Finlandia Hall

Monday, June 4, 2018

8:30-9:50 Plenary session IISponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Finlandia Main HallChairs: Hellmut Augustin & Luisa Iruela-Arispe8:30-9:10 Elisabetta Dejana (Milan, Italy & Uppsala, Sweden) Transcriptional regulation of the brain microvasculature9:10-9:50 Gou Young Koh (Daejeon, Korea) Organotypic vasculatures: maintenance and pathophysiology

9:50-10:15 Coffee Break

Parallel sessions 1-4

10:15-12:15 Parallel session 1: AtherosclerosisSponsored by the Japanese Vascular Biology and Medicine Organisation

Helsinki HallChairs: Yvonne Alexander & Petri Kovanen10:15-10:45 Klaus Ley (La Jolla, CA, USA) T cell immune response in atherosclerosis10:45-11:15 Masayuki Yoshida (Tokyo, Japan) A novel role of neutrophils in vascular inflammation and atherosclerosis induced by high fat diet11:15-11:45 Tetsuya Matoba (Fukuoka, Japan) Role of oxysterols in endothelial dysfunction and atherothrombosis11:45-12:00 Short talk: Yun Fang (Chicago, IL, USA) Coronary artery disease locus 1p32.2 harbors a flow-sensitive endothelial enhancer that regulates PLPP312:00-12:15 Short talk: Kim Pin Yeo (Singapore, Singapore) Aortic lymphatic vessel: for or against atherosclerosis in experimental models?

– Sunday – Monday

Program

– 18 –

IVBM2018Program

10:15-12:15 Parallel session 2: Blood brain barrierVeranda 1Chairs: Jean-Leon Thomas & Berislav Zlokovic10:15-10:45 Calvin Kuo (Stanford, CA, USA) Molecular regulation of the blood-brain barrier10:45-11:15 Berislav Zlokovic (Los Angeles, CA, USA) Alzheimer’s disease: A matter of dysfunction of the blood-brain barrier?11:15-11:45 Injune Kim (Daejeon, Korea) Signalings for adult blood-retina barrier maintenance11:45-12:00 Short talk: Patric Turowski (London, UK) VEGF receptor signalling in the leaky neural endothelium12:00-12:15 Short talk: Christian Ramakers (Leiden, The Netherlands) BBB on-a-chip: a 3D in vitro model of the human blood brain barrier (BBB)

10:15-12:15 Parallel session 3: TIE2 pathway in vascular diseaseSponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Veranda 2Chairs: Samir Parikh & Susan Quaggin10:15-10:45 Hellmut Augustin (Heidelberg, Germany) Mechanisms of vascular maturation and quiescence10:45-11:15 Pipsa Saharinen (Helsinki, Finland) New mechanisms of vascular leakage11:15-11:45 Dietmar Vestweber (Münster, Germany) Mechanisms that regulate leukocyte diapedesis and endothelial junctions11:45-12:00 Short talk: Sarah Mueller (Durham, NC, USA) The scaffolding protein Caskin2 regulates vascular homeostasis downstream of Angiopoietin/ Tie receptor signaling11:45-12:00 Short talk: Elizabeth Jones (Leuven, Belgium) Shear stress and VE-cadherin: The molecular mechanism of vascular fusion

10:15-12:15 Parallel session 4: Metabolic diseaseSponsored by Novo Nordisk

Veranda 3Chairs: Zoltan Arany & Kenneth Walsh10:15-10:45 Andreas Fischer (Heidelberg, Germany) Endothelial control of muscle cell metabolism10:45-11:15 Hyo-Soo Kim (Seoul, Korea) Resistin - Cap1 axis in the pathogenesis of metabolic syndrome 11:15-11:45 Ulf Eriksson (Stockholm, Sweden) Role of VEGF-B signaling in diabetic complications11:45-12:00 Short talk: Xuri Li (Guangzhou, China) Novel function of VEGF-B in tethering the FGF2/FGFR1 pathway12:00-12:15 Short talk: Peppi Koivunen (Oulu, Finland) Lower hemoglobin levels associate with lower body mass index and healthier metabolic profile

12:15-12:45 Lunch

– Monday

– 19 –

IVBM2018Program

12:30-13:00 Lunch SeminarSponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Chair: Kevin Peters (Cincinnati, OH, USA)Peter Campochiaro (Baltimore, MD, USA)Targeting the Tie2 pathway for retinal and choroidal vascular diseases

12:45-14:15 Poster session I


14:15-16:00 Parallel session 5: Vascular inflammationHelsinki HallChairs: Jozef Dulak & Dietmar Vestweber14:15-14:45 Beat Imhof (Geneve, Switzerland) Novel mechanisms in acute and chronic vascular inflammation14:45-15:15 Sirpa Jalkanen (Turku, Finland) New tools to prevent vascular leakage15:15-15:45 Britta Engelhardt (Bern, Switzerland) Brain barriers control immune surveillance of the CNS15:45-16:00 Short talk: Jennifer Gamble (Sydney, Australia) Therapeutic manipulation of VE-cadherin

14:15-16:00 Parallel session 6: Mechanotransduction & ECMVeranda 1Chairs: Tatiana Byzova & Claudio Franco14:15-14:45 Stefan Offermanns (Bad Nauheim, Germany) GPCRs and downstream signaling in endothelial mechanotransduction14:45-15:15 Martin A. Schwartz (New Haven, CT, USA) Fluid shear stress in endothelial phenotype and function15:15-15:45 Yu Huang (Hong Kong, China) Endothelial mechanical stress, inflammation and atherogenesis15:45-16:00 Short talk: Anne-Clemence Vion (Nantes, France) Primary cilia sensitize endothelial cells to BMP and prevent excessive vascular regression

14:15-16:00 Parallel session 7: Vessel development & stabilitySponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Veranda 2Chairs: Christopher Kontos & Anna Randi14:15-14:45 Samir Parikh (Boston, MA, USA) Coagulation and hemostasis during inflammation14:45-15:15 Yvonne Reiss (Frankfurt am Main, Germany) Improved survival in a glioblastoma model by a combination of anti-angiogenic and immune checkpoint therapy15:15-15:45 Yulong He (Jiangsu, China) Tie2 in the regulation of angiogenesis and lymphatic formation15:45-16:00 Short talk: Lauri Eklund (Oulu, Finland) Venous specific development and fluid homeostasis in the retina

– Monday

– 20 –

IVBM2018Program

14:15-16:00 Parallel session 8: Lymphatic specification & morphogenesisVeranda 3Chairs: Dontscho Kerjaschki & Taija Mäkinen14:15-14:45 Guillermo Oliver (Chicago, IL, USA) Lumen formation and maintenance in the lymphatic vasculature14:45-15:15 Natasha Harvey (Adelaide, Australia) Dissecting gene function in lymphatic vessel morphogenesis15:15-15:45 Friedemann Kiefer (Münster, Germany) Importance of VE-cadherin in the maintenance of specific lymphatic vessel beds15:45-16:00 Short talk: Michael Jeltsch (Helsinki, Finland) All you ever wanted to know about vascular endothelial growth factor-C processing


16:30-17:50 Plenary session IIICo-sponsored by Aerpio Pharmaceuticals - Targeting the Tie2 pathway for novel therapeutics

Finlandia Main HallChairs: Ralf Adams & Debabrata Mukhopadhyay16:30-17:10 Holger Gerhardt (Berlin, Germany) Principles and regulation of endothelial cell dynamics in angiogenesis17:10-17:50 Naoki Mochizuki (Osaka, Japan) Ang1/Ang2-Tie1/Tie2 signaling for hematovascular development in zebrafish

18:30 Reception at Helsinki City Hall

Tuesday, June 5, 2018

8:30-9:50 Plenary session IVFinlandia Main HallChairs: Jan Kitajewski & Curzio Rüegg8:30-9:10 Anne Eichmann (New Haven, CT, USA), The EMBO Keynote Lecture Guidance of organ-specific vascular patterning9:10-9:50 Rakesh Jain (Boston, MA, USA) Reengineering the tumor microenvironment to improve cancer treatment: Bench to bedside



10:15-12:15 Parallel session 9: Neurovascular interactions & diseaseHelsinki HallChairs: Christer Betsholtz & Britta Engelhardt10:15-10:45 Jaime Grutzendler (New Haven, CT, USA) In vivo optical interrogation of neurovascular function and pathology10:45-11:15 Chenghua Gu (Boston, MA, USA) Interactions of nervous and vascular systems11:15-11:45 Jonathan Kipnis (Charlottesville, VA, USA) Meningeal lymphatic network in CNS pathologies11:45-12:00 Short talk: Bong-Ihn Koh (Daejeon, Korea) Brain photothrombotic injury induces VEGF-dependent pathologic angiogenesis and sustained vascular leakage12:00-12:15 Short talk: Laurent Jacob (Paris, France) Volume imaging of the rachis lymphatic network in rodents

– Monday – Tuesday

– 21 –

IVBM2018Program

10:15-12:15 Parallel session 10: Endothelial cell metabolism & angiogenesisVeranda 1Chairs: Riikka Kivelä & William Sessa10:15-10:45 Zoltan Arany (Philadelphia, PA, USA) The peculiarities of endothelial metabolism10:45-11:15 Michael Potente (Bad Nauheim, Germany) Metabolite signalling in the vascular endothelium11:15-11:45 Peter Carmeliet (Leuven, Belgium) Angiogenesis revisited: role and (therapeutic) implications of endothelial metabolism11:45-12:00 Short talk: Bernard M. van den Berg (Leiden, the Netherlands) Endothelial glucose metabolism regulates glycocalyx hyaluronan synthesis and thereby vessel stability12:00-12:15 Short talk: Debabrata Mukhopadhyay (Jacksonville, FL, USA) Neuropilin-1 maintains dimethylarginine dimethylaminohydrolase 1 expression in endothelial cells and regulates angiotensin II induced-hypertension

10:15-12:15 Parallel session 11: Vascular SignallingSponsored by Eli Lilly

Veranda 2Chairs: Xuri Li & Lena Claesson-Welsh10:15-10:45 Young-Guen Kwon (Seoul, Korea) CLEC14A in regulation of VEGFR-dependent signals in the vasculature10:45-11:15 Tetsuro Watabe (Tokyo, Japan) TGF-β family signals in the formation and maintenance of vascular systems11:15-11:45 Lars Jakobsson (Stockholm, Sweden) Endoglin in regulation of vascular patterning and malformation11:45-12:00 Short talk: Emma Gordon (St. Lucia, Australia) Dynamic cell rearrangements guiding vascular growth and stability12:00-12:15 Short talk: Suk-won Jin (New Haven, CT, USA) ACVR1/ALK2 enables venous selective pro-angiogenic responses to BMP signaling

10:15-12:15 Parallel session 12: Targeting tumor vasculatureSponsored by The Swedish Childhood Cancer Foundation

Finlandia Main HallChairs: Sudhakar Chintharlapalli & Yvonne Reiss10:15-10:45 Michele De Palma (Lausanne, Switzerland) Reprogramming tumor blood vessels for enhancing cancer immunotherapy10:45-11:15 Gabriele Bergers (Leuven, Belgium) High-endothelial venules in cancer11:15-11:45 Donald McDonald (San Francisco, CA, USA) Vascular targeting by oncolytic vaccinia virus11:45-12:00 Short talk: Stephen Moss (London, UK) Pre-clinical development and testing of Magacizumab, a therapeutic antibody against LRG112:00-12:15 Short talk: Radu V. Stan (Hanover, NH, USA) Plasmalemma vesicle associated protein (PLVAP) is a novel target for cancer immunotherapy

12:15-12:45 Lunch

12:45-14:15 Poster session II

– Tuesday

– 22 –

IVBM2018Program


14:15-16:15 Parallel session 13: Cardiovascular diseaseHelsinki HallChairs: Michael Simons & Seppo Ylä-Herttuala14:15-14:45 Riikka Kivelä (Helsinki, Finland) Paracrine regulation of endothelial-cardiomyocyte crosstalk in cardiac hypertrophy14:45-15:15 Kenneth Walsh (Charlottesville, VA, USA) Somatic mutations that drive clonal hematopoiesis and vascular disease15:15-15:45 Stefanie Dimmeler (Frankfurt am Main, Germany) Regulation of vascular growth by non-coding RNAs15:45-16:00 Short talk: Thomas Korff (Heidelberg, Germany) NFAT5/TonEBP - a mechanosensitive transcription factor in vascular smooth muscle cells controlling arterial remodeling16:00-16:15 Short talk: Claudio Franco (Lisbon, Portugal) Junctional forces and wall shear stress compete to coordinate collective endothelial cell polarity

14:15-16:15 Parallel session 14: Vascular smooth muscle cellsOrganized in collaboration with European Society of Cardiology

Veranda 1Chairs: Marie-Luce Bochaton-Piallat & Magnus Bäck14:15-14:45 Cecilia Giachelli (Seattle, WA, USA) Vascular calcification: new concepts in regulation and therapy14:45-15:15 Gordon Francis (Vancouver, Canada) Smooth muscle cells: The silent majority of atherosclerotic lesion foam cells15:15-15:45 Gary Owens (Charlottesville, VA, USA) IL1b signaling in smooth muscle cells plays a critical role in atherosclerotic lesion pathogenesis15:45-16:00 Short talk: Muriel Laffarque (Toulouse, France) PI3Kγ-dependent T cell response delays endothelial healing and reveals a novel role for arterial CXCL1016:00-16:15 Short talk: Angela Bradshaw (Glasgow, UK) TGFβ signaling via ALK1 and ALK5 regulates distinct functional pathways in vein graft intimal hyperplasia

16:30-18:30 European Society of Cardiology round tableVeranda 1

14:15-16:15 Parallel session 15: LymphangiogenesisVeranda 2Chairs: Agnes Noel & Tatiana Petrova14:15-14:45 Taija Mäkinen (Uppsala, Sweden) Mechanisms of sprouting lymphangiogenesis14:45-15:15 Stefan Schulte-Merker (Münster, Germany) Functional analysis of brain lymphatic endothelial cells15:15-15:45 Ben Hogan (Brisbane, Australia) New mechanisms of lymphatic vascular development from zebrafish15:45-16:00 Short talk: Raghu Kataru (New York, NY, USA) Critical role of tumor lymphatic function in regulating tumor inflammatory and immunosuppressive microenvironment16:00-16:15 Short talk: Akira Takeda (Turku, Finland) A new type of lymphatic endothelial cells in the medulla of lymph nodes

– Tuesday

– 23 –

IVBM2018Program

14:15-16:15 Parallel session 16: Tumor angiogenesisSponsored by The Swedish Childhood Cancer Foundation

Finlandia Main HallChairs: Anna Dimberg & Eli Keshet14:15-14:45 Gavin Thurston (Tarrytown, NY, USA) Delta-Notch interactions between stromal cells and tumor cells14:45-15:15 Nobuyuki Takakura (Osaka, Japan) Vascular promotion by LPA4 activation improves the malignant tumor microenvironment15:15-15:45 Kristian Pietras (Lund, Sweden) Blood vessel control of the malignant phenotype15:45-16:00 Short talk: Amanda Lund (Portland, OR, USA) IFNγ-dependent activation of dermal lymphatic vessels limits cytotoxic immunity in malignant and inflamed skin16:00-16:15 Short talk: Giorgio Seano (Paris, France) In vivo dynamics and targeting of vessel co-option in glioblastoma


16:45-18:05 Plenary session VFinlandia Main HallChairs: Stephane Germain & Mark Kahn16:45-17:25 William Sessa (New Haven, CT, USA) The interfaces of endothelial function and lipid metabolism17:25-18:05 Ralf Adams (Münster, Germany) Vascular cell heterogeneity and functional specialization

18:10-19:10 ShowcasesVeranda 218:10-18:40 Pelle Larshammar, Bio-Rad Laboratories Using Droplet Digital™ PCR (ddPCR™) for Cancer and Liquid Biopsy Studies18:40-19:10 Jean Habyarimana, Janvier Labs Breeder’s expertise and its contribution in cardio and vascular research

18:10-19:10 Meet the EditorsHelsinki Hall

Wednesday, June 6, 2018

8:30-9:50 Plenary session VIFinlandia Main HallChairs: Elisabetta Dejana & Vesa Kiviniemi8:30-9:10 Maiken Nedergaard (Copenhagen, Denmark & Rochester, NY, USA) The glymphatic system9:10-9:50 Mark Kahn (Philadelphia, PA, USA) Signaling pathways in vascular disease


– Tuesday – Wednesday

– 24 –

IVBM2018Program


10:15-12:15 Parallel session 17: Leukocyte trafficking & endothelial barrier functionHelsinki HallChairs: Jennifer Gamble & David Jackson10:15-10:45 Cornelia Halin (Zurich, Switzerland) Leukocyte migration through afferent lymphatic vessels10:45-11:15 Jaap van Buul (Amsterdam, The Netherlands) How leukocytes cross the endothelium: the actin link11:15-11:30 Short talk: Masataka Majima (Kanagawa, Japan) Microenvironmental BLT1-signaling facilitates tumor-associated angiogenesis via inducing mast cell recruitment11:30-11:45 Short talk: William A. Muller (Chicago, IL, USA) The role of the PECAM/VE-cadherin/VEGFR2 mechanosensing complex in initiating transendothelial migration11:45-12:00 Short talk: Arie Horowitz (Philadelphia, PA, USA) MPDZ trafficking underlies endothelial cell junction dynamics12:00-12:15 Short talk: Mark Richards (Uppsala, Sweden) Identification of permeability permissive vessels and their molecular markers using correlative intravital imaging

10:15-12:15 Parallel session 18: Novel functions of lymphatic vesselsVeranda 1Chairs: Mark Achen & Jörg Wilting10:15-10:45 Barbara Garmy-Susini (Toulouse, France) Lymphatic system: a novel actor in cancer-associated cachexia10:45-11:15 Ebba Brakenhielm (Rouen, France) Cardiac lymphangiogenesis in cardiovascular diseases11:15-11:45 Dontscho Kerjaschki (Vienna, Austria) Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice11:45-12:00 Short talk: Timothy Padera (Cambridge, MA, USA) Lymph node metastases as a source for distant metastases12:00-12:15 Short talk: Agnès Noel (Liège, Belgium) uPARAP/endo180: a novel partner of VEGFR-2/R-3 that controls VEGF-C-induced lymphatic sprouting

10:15-12:15 Parallel session 19: AngiogenesisVeranda 2Chairs: Holger Gerhardt & Valentin Djonvo10:15-10:45 Victoria Bautch (Chapel Hill, NC, USA) How blood vessels control their destiny10:45-11:15 Yoshiaki Kubota (Tokyo, Japan) Cell-to-cell communication in retinal vascular development11:15-11:45 Rui Benedito (Madrid, Spain) High mitogenic stimulus induced by VEGF or Notch inhibition arrests angiogenesis11:45-12:00 Short talk: Alessandro Fantin (London, UK) Erythro-myeloid progenitors contribute endothelial cells to developing vasculature12:00-12:15 Short talk: Osamu Nakagawa (Osaka, Japan) Significance of the Hey family of transcription factors during cardiovascular development

– Wednesday

– 25 –

IVBM2018Program

10:15-12:15 Parallel session 20: Mechanisms of vascular diseaseVeranda 3Chairs: Andreas Bikfalvi & Karen Hirschi10:15-10:45 Michael Dellinger (Dallas, TX, USA) Lymphatic vessels and vanishing bones: characterization of an animal model of Gorham-Stout disease10:45-11:15 Mariona Graupera (Barcelona, Spain) Role of oncogenic PI3K in endothelium-related diseases11:15-11:45 Goo Taeg Oh (Seoul, Korea) Atherogenesis protection by a novel cytokine produced by alternatively activated macrophages11:45-12:00 Short talk: Andrea Banfi (Basel, Switzerland) EphrinB2/EphB4 signaling regulates non-sprouting angiogenesis by VEGF12:00-12:15 Short talk: Mia Phillipson (Uppsala, Sweden) Perivascular macrophages regulate blood flow following tissue damage

12:15-12:45 Lunch

12:45-14:15 Poster session III


14:15-16:00 Parallel session 21: Organotypic vasculatureHelsinki HallChairs: Natasha Harvey & Gou Young Koh14:15-14:45 Bin Zhou (Shanghai, China) Genetic targeting of organ specific endothelial cells14:45-15:15 Tatiana Petrova (Lausanne, Switzerland) Organ-specific features and control of lymphatic vasculature15:15-15:45 Karina Yaniv (Rehovot, Israel) Differentiation of endothelial cells and formation of organ-specific vascular beds15:45-16:00 Short talk: Mahak Singhal (Heidelberg, Germany) Endothelial cell fitness dictates the source of regenerating liver vasculature

14:15-16:00 Parallel session 22: Endothelial regeneration & senescenceVeranda 1Chairs: Lauri Eklund & Shahin Rafii14:15-14:45 Jun K. Yamashita (Kyoto, Japan) Blood vessels for tissue regeneration14:45-15:15 Luisa Iruela-Arispe (Los Angeles, CA, USA) Molecular mechanisms of endothelial regeneration15:15-15:45 Mike Sapieha (Montreal, Canada) Cellular senescence and angiogenesis15:45-16:00 Short talk: Mei Xin (Cincinnati, OH, USA) Hippo signaling effector Yap regulates hyaloid vasculature regression in the developing eye

– Wednesday

– 26 –

IVBM2018Program

14:15-16:00 Parallel session 23: Vascular physiology & pathologyVeranda 2Chairs: Timothy Hla & Levon Khachigian14:15-14:45 Ingrid Fleming (Frankfurt am Main, Germany) Inhibition of soluble epoxide hydrolase stabilizes endothelial cell-pericyte interactions and prevents diabetic retinopathy14:45-15:15 Randall S Johnson (Cambridge, UK & Stockholm, Sweden) The role of hypoxic response in vascular function15:15-15:45 Helge Wiig (Bergen, Norway) Extrarenal interstitial sodium storage in extracellular volume and blood pressure homeostasis15:45-16:00 Short talk: Leigh Coultas (Victoria, Australia) ‘Vessel reassembly’ in the absence of endothelial apoptosis as a mechanism for revascularising ischemic retinas

14:15-16:00 Parallel session 24: Epigenetics & genetics of vascular differentiationVeranda 3Chairs: Graeme Birdsey & Risto Kerkelä14:15-14:45 Michael Detmar (Zurich, Switzerland) Epigenetic control of vascular differentiation and function14:45-15:15 Anna Randi (London, United Kingdom) Transcriptional and epigenetic control of endothelial and tissue homeostasis15:15-15:30 Short talk: Stefania Nicoli (New Haven, CT, USA) MicroRNA-dependent regulation of biomechanical genes establish tissue stiffness homeostasis15:30-15:45 Short talk: Minna Kaikkonen-Määttä (Kuopio, Finland) Developmentally regulated chromatin interactions orchestrate transcriptional changes in endothelial cells during vasculogenesis and angiogenesis15:45-16:00 Short talk: Ilse Luyckx (Antwerpen, Belgium) SMAD2 and SMAD6: two novel genetic players in aortic aneurysm and dissection


16:30-18:50 Plenary session VII & WorkshopFinlandia Main HallChairs: Gary Owens & Nobuyuki Takakura16:30-17:10 Michael Simons (New Haven, CT, USA) Disease pathogenesis and cell fate: the tale of two cell types17:10-18:40 Workshop on Vascular Single-Cell RNA Sequencing Investigators from the vascular biology field will present their latest results and discuss technological challenges and bioinformatics methods in single-cell RNA sequencing.17:10-17:40 Sten Linnarsson (Stockholm, Sweden) Inferring cell types and lineages of the mammalian brain from single-cell transcriptomes17:40-17:55 Christer Betsholtz (Uppsala, Sweden) Defining mural cell types by single cell RNA sequencing17:55-18:10 Short talk: Kevin Brulois (Stanford, CA, USA) Single-cell transcriptomics of lymphoid tissue blood endothelial cells18:10-18:25 Short talk: Qi Zhao (Tarrytown, NY, USA) Sequencing tumor endothelial cells with 10x Genomics single cell platform18:25-18:40 Short talk: Michael Vanlandewijck (Uppsala, Sweden) Blood-brain barrier single-cell transcriptomics with SmartSeq218:40-18:50 Presentation of IVBM2020 in Seoul Hyo-Soo Kim & Gou Young Koh

19:00- Nordic Night at Allas Sea Pool

– Wednesday

– 27 –

IVBM2018Program

Thursday, June 7, 2018


8:30-9:30 Parallel session 25: Vascular anomaliesHelsinki HallChairs: Michael Dellinger & Mariona Graupera8:30-9:00 Joyce Bischoff (Boston, MA, USA) GNAQ mutant endothelial cells in capillary malformations9:00-9:30 Miikka Vikkula (Brussels, Belgium) Signaling defects in fast-flow vascular anomalies

8:30-9:30 Parallel session 26: Clinical translationSponsored by Herantis Pharma

Veranda 1Chairs: Andrea Banfi & Michael Detmar8:30-9:00 Seppo Ylä-Herttuala (Kuopio, Finland) VEGFs in therapeutic vascular growth and beyond9:00-9:30 Anne Saarikko (Helsinki, Finland) New therapeutic tools for lymphedema treatment

8:30-9:30 Parallel session 27: ArteriogenesisVeranda 2Chairs: Victoria Bautch & Jun Yamashita8:30-9:00 Kristy Red-Horse (Stanford, CA, USA) Arteriogenesis during cardiac development and injury9:00-9:30 Ferdinand Le Noble (Karlsruhe, Germany) Flt1 determines lumen formation during arteriogenesis

8:30-9:30 Parallel session 28: Fluid shear stress regulationVeranda 3Chairs: Injune Kim & Martin Schwartz8:30-9:00 Young-Kwon Hong (Los Angeles, CA, USA) Regulation of lymphatic development by fluid flow9:00-9:30 Arndt Siekmann (Münster, Germany) Investigating the role of hemodynamic forces in embryonic blood vessel patterning


10:00-12:30 Plenary session VIIISponsored by Regeneron Pharmaceuticals

Finlandia Main Hall

10:00-10:20 Poster/Travel awards ceremony, awards sponsored by LE&RN, NAVBO, EVBO, French Angiogenesis Society, EMBO Molecular Medicine, JVBMO & Wihuri Research InstituteChairs: Naoki Mochizuki & Bin Zhou10:20-11:00 Shahin Rafii (New York, NY, USA) Molecular determinants of vascular heterogeneity development11:00-11:40 Didier Stainier (Bad Nauheim, Germany) Vascular development in zebrafish and mouse11:40-12:20 Timothy Hla (Boston, MA, USA) Signaling and gene expression mechanisms of endothelial injury

12:20-12:30 Closing words

– Thursday

Posters – Monday

– 28 –

IVBM2018

M001

Systematic pharmacological suppression uncovers novel molecular pathways involved in cerebral cavernous malformations

Cécile Otten1, Jessica Knox2,7, Gwénola Boulday3,8, Mathias Eymery4, Martin Neuenschwander5, Ingo Vogt6, Peter Roy2, Corinne Albiges-Rizo4, Eva Faurobert4, Jens von Kries5, Mónica Campillos6, Elisabeth Tournier-Lasserve3,8, Brent Derry2,7, Salim Abdelilah-Seyfried1,9

1Biochemistry and Biology, Potsdam University, Potsdam, Germany, 2Department of Molecular Genetics, University of Toronto, Ontario, 3Université Paris Diderot, Génétique et physiopathologie des maladies cérébro-vasculaires, Paris, France, 4Université Grenoble Alpes, Institute for Advanced Biosciences, Grenoble, France, 5Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Berlin, Germany, 6German Center for Diabetes Research, Neuherberg, Germany, 7Developmental and Cell Biology Program, The Hospital for Sick Children, Ontario, Toronto, Canada, 8AP-HP, Groupe hospitalier Saint-Louis, Lariboisière, Fernand-Widal, Service de génétique moléculaire neuro-vasculaire, Paris, France, 9Institute of Molecular Biology, Hannover Medical School, Hannover, Germany

• We screened 5268 unique small-molecules to suppress cerebral cavernous malformation phe-notypes in mutant worm, zebrafish, mouse, or human endothelial cells.

• Systems biology-based target prediction tools revealed signaling pathways relevant to the disease and potential targets for small-mole-cule-based therapies.

• Indirubin-3-monoxime suppressed the loss-of- CCM phenotypes in several CCM mutant models.

M002

Fetal Breathing Movements and Pulmonary Lymphatics Function Together to Prepare the Lung for Inflation

Kitti Ajtay1,2, Mark L. Kahn3, Josef Penninger4, Zoltán Jakus1,2

1Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary, 2MTA-SE „Lendület” Lymphatic Physiology Research Group, Budapest, Hungary, 3University of Pennsylvania, Perelman School of Medicine, Philadelphia, USA, 4Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria

• We have revealed the previously unrecognized role of fetal breathing movements (FBMs) in pre-natal lung expansion

• The lack of FBMs results in impaired prenatal pul-monary lymphatic function, while does not influ-ence molecular lung development

• Our results suggest that FBMs and prenatal pul-monary lymphatics function together to prepare the developing lung for inflation at birth

M003

Retinal neurovascular coupling arises at cap-illaries, which show opposite-synchronized responses

Luis Alarcon-Martinez1, Deborah Villafranca-Baughman1, Adriana Di Polo1

1University Of Montreal Hospital Research Center (CRCHUM), Montreal, Canada

• A new approach to study neurovascular coupling in the retina

• Retinal neurovascular coupling occurs at capillary level

• Light-evokedcapillaryresponseareoppositeandsynchronized

M004

Piezo1 and Gq/G11 promote endothelial inflammation and atherosclerosis depending on the flow pattern

Julian Albarran-Juarez1, Till Althoff1,2, Andras Iring1, ShengPeng Wang1, Myriam Grimm1, Boris Strilic1, Nina Wettschureck1,3, Stefan Offermanns1,3

1Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany, 2Charité Department of Cardiology and Vascular Medicine, Berlin, Germany, 3Centre for Molecular Medicine, Medical Faculty, J.W. Goethe University Frankfurt, Frankfurt, Germany

• Piezo1 and Gq/G11-mediated downstream sig-naling processes are involved in endothelial mechanosignaling by primarily sensing flow intensity independently of the flow direction.

• In cells exposed to disturbed flow integrins are activated in a Piezo1-Gq/G11-dependent manner resulting in FAK-mediated NF-kB activation and pro-inflammatory effects.

• Differential activation of integrin signaling by flow represents an important approach to modulate atheroprotection.

Posters

Posters – Monday

– 29 –

IVBM2018

M005

Importance of interplay between endothelial progenitor cells and platelets during athero-sclerosis in a vitro model

Nicoleta Alexandru1, Sabina Frunza2, Emanuel Dragan1, Elisabeta Bãdilã2,3, Alina Constantin1, Miruna Nemecz1, Gabriela Tanko1, Habil Adriana Georgescu1

1Institute of Cellular Biology and Pathology ‘Nicolae Simionescu’ of the Romanian Academy, Bucharest, Romania, 2Internal Medicine Clinic, Emergency Clinical Hospital, Bucharest, Romania, 3’Carol Davila’ University of Medicine and Pharmacy, Bucharest, Romania

• In vitro exposure to platelets of healthy origins had a positive effect on functional properties of atherosclerotic late EPCs.

• The most likely candidates mediating EPC-plate-let interaction could be SDF-1alpha, VEGF, PDGF, CD40L, IL-1β,-6,-8, miR-223 and IGF-1R.

• Results lead to new perspective in using EPC for both repair and maintenance of existing vascula-ture within the body, and for cardiovascular dis-ease treatment.

M006

Vascular defects of the retinal vasculature in a mouse model of marfan syndrome

Florian Alonso1, M Thierry Dakhli2, Elisabeth Génot1

1University Of Bordeaux - Inserm U1045, Bordeaux, France, 2Inserm UMS001, Bordeaux, France

• In Marfan syndrome (MFS), defective fibrillin microfibrils affect elastic and non elastic tissues leading to vascular and ocular defects.

• By confocal imaging on whole mounted retinas from MFS mice, we have identified vascular alter-ations at developmental and adult stages.

• The alterations detected in MFS mouse reti-nas may compromise microvascular functions, thereby contributing to ocular complications.

M007

Investigating the role of Cdc42 in mural cells

Alberto Alvarez-Aznar1, Ralf Adams2, Cord Brakebusch3, Christer Betsholtz1,4, Konstantin Gaengel1

1Uppsala University, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala, Sweden, 2Max Plank Institut for Molecular Medicine, Department of Tissue Morphogenesis, Münster, Germany, 3University of Copenhagen, BRIC, Copenhagen , Denmark, 4Integrated Cardio Metabolic Centre, Karolinska Institutet, Novum, Huddinge, Sweden

• Deletion of Cdc42 in mural cells using PDG-FR-beta ERT2Cre leads to changes in vascular pat-terning at different developmental stages

• The P7 vasculature appears disorganized with regional changes in vascular density and cross-over of capillaries, this phenotype resolves before P28

• At P28 the vascular branching becomes altered, showing a reduction in branching angles of arte-rioles

M008

Modeling congenital heart disease with patient-derived induced pluripotent stem cells

Minna Ampuja1, Emmi Helle1,3, Diego Balboa2, Solja Eurola2, Tiina Ojala3, Timo Otonkoski2, Riikka Kivelä1

1Research Programs Unit, Translational Cancer Biology Program, Faculty of Medicine, University of Helsinki, and Wihuri Research Institute, Helsinki, Finland, 2Research Programs Unit, Molecular Neurology and Biomedicum Stem Cell Centre, Faculty of Medicine, University of Helsinki, Helsinki, Finland, 3Helsinki University Children’s Hospital, University of Helsinki, Helsinki, Finland

• We are studying a new candidate gene variant potentially causing hypoplastic left heart syn-drome (HLHS).

• We generated knockout and heterozygous mutants of the gene in control iPSCs by CRISPR/Cas9.

• HLHS-patient-derived, knockout and heterozy-gous iPSCs were successfully differentiated into cardiac and endothelial cells, which will be used to study the pathogenic role of the gene in HLHS.

Posters – Monday

– 30 –

IVBM2018

M009

Effect of cardiovascular risk factors and heart failure on cardiac endothelial cell transcrip-tome

Karthik Amudhala Hemanthakumar1,2, Shentong Fang1,2, Eero Mervaala3, Riikka Kivelä1,2

1Wihuri Research Institute, Biomedicum Helsinki, Finland, 2Translational Cancer Biology Program, Faculty of Medicine, University of Helsinki, Biomedicum Helsinki, Finland, 3Department of Pharmacology, Faculty of Medicine, Biomedicum Helsinki, University of Helsinki, Finland

• Effects of exercise training and pathological CVD risk factors (ageing, obesity and TAC) on cardiac endothelial cell transcriptome were studied.

• Exercise increased and pathological stimuli decreased endothelial cell number and all inter-ventions induced significant changes on the car-diac EC transcriptome.

• We have identified genes, which were affected by several treatments, and changed to opposite directions by physiological and pathological stim-uli.

M010

Single cell RNA sequencing studies on peri-cyte-deficient blood-brain barrier

Maarja Andaloussi Mäe1, Liqun He2, Michael Vanlandewijck3, Khayrun Nahar1, Annika Keller4, Christer Bestholtz1,3

1Uppsala University, Uppsala, Sweden, 2Tianjin Neurological Institute, Tianjin, China, 3Karolinska Institute, Stockholm, Sweden, 4Zürich University, Zürich, Switzerland

• Pericyte-deficient Pdgfb ret/ret mouse is a model for several human brain disease-related pro-cesses.

• Single cell RNA sequencing analyses revealed extensive endothelial cell heterogeneity in peri-cyte-deficient brain vasculature.

• Data analysis together with immunofluorescence stainings have been helpful in characterizing the pathologic phenotypes found in pericyte-defi-cient vasculature.

M011

Early developmental induction of vascular mural cell lineage requires Notch signaling

Koji Ando1, Shigetomo Fukuhara2, Naoki Mochizuki3,4, Christer Betsholtz1,5

1Uppsala Univ., Dept. IGP, Rudbeck Lab., Uppsala, Sweden, 2Dept. of Mol. Pathophysiol., Nippon Medical Sch. Japan, Kawasaki, Japan, 3Dept. Cell Biol., Natl. Cerebr. & Cardiovasc. Ctr. Res. Inst., Suita, Japan, 4AMED-CREST, Natl. Cerebr. & Cardiovasc. Ctr. Res. Inst., Suita, Japan, 5Integrated Cardio Metab. Ctr, Karolinska Inst., Huddinge, Sweden

• Description of mural cell (MC) development in zebrafish utilizing MC-reporter lines.

• pdgfrb-high/abcc9+ cells of the MC lineage emerge from peri-arterial naïve pdgfrb-low/abcc9- mesenchymal cells during 36-72 hours post-fertilization.

• Genetic intervention tools revealed that Notch2/3 activation in precursors during differen-tiation periods is indispensable for the differenti-ation into MCs.

M012

Characterisation of perivascular PDGFR-alpha positive mesenchymal cells in meninges and cns

Johanna Andrae1, Michael Vanlandewijck1,2, Maarja Andaloussi Mäe1, Liqun He3, Christer Betsholtz1,2

1Uppsala University, Uppsala, Sweden, 2Integrated Cardio Metabolic Centre/Karolinska Institutet, Huddinge, Sweden, 3Tianjin Medical University General Hospital, Tianjin, China

• Fibroblast-like cells expressing PDGFR-alpha are present along blood vessels in the cns.

• The cells are located between the vascular smooth muscle cells and the astrocyte endfeet.

• 3. Single cell sequencing data imply that there are several subgroups of perivascular fibroblasts.

Posters – Monday

– 31 –

IVBM2018

M013

A new model of guided self-organization allowing rapid formation of functional vessels

Laetitia Andrique1, Gaelle Recher2, Kevin Alessandri2, Nadege Pujol1, Maxime Feyeux2, Pierre Nassoy2, Andreas Bikfalvi1

1Inserm U1029, Pessac, France, 2Institut d’Optique d’Aquitaine LP2N UMR5298, talence, France

• Use of microfluidic device in vascular tissue engi-neering

• Artificial vessels that preserve main properties of mature blood vessels. Revelant model for angio-genesis study.

• Relevant model for vascular graft

M014

Loss of angiopoietin receptor activates YAP/TAZ and a mesenchymal gene set in ECs

Andrey Anisimov1,4, Emilia Korhonen1,4, Pipsa Saharinen1,4, Susan Quaggin2, Marie Jeansson3, Kari Alitalo1,4

1University Of Helsinki, Helsinki, Finland, 2Feinberg Cardiovascular Research Institute and Division of Nephrology and Hypertension, Northwestern University, Chicago, USA, 3Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 4Wihuri Research Institute, Biomedicum Helsinki,, Helsinki, Finland

• Tie2 silencing in cultured endothelial cells results in endothelial-to-mesenchymal transition.

• Tie2 silencing led to activation of the major Hippo downstream effectors YAP and TAZ.

• Immunohistochemical analysis of mouse tissues conditionally deleted of Tie2 revealed YAP/TAZ activation and upregulation of the mesenchymal marker vimentin, mirroring the changes upon downregulation of Tie2 at the vascular front in developing retina.

M015

Development and plasticity of meningeal lym-phatic vessels

Salli Antila1, Sinem Karaman1, Harri Nurmi1, Mikko Airavaara2, Merja Voutilainen2, Thomas Mathivet3, Dmitri Chilov1, Zhilin Li1, Tapani Koppinen1, Jun-Hee Park4, Shentong Fang1, Aleksanteri Aspelund1, Mart Saarma2, Anne Eichmann3,5,6, Jean-Léon Thomas4,7, Kari Alitalo1

1Wihuri Research Institute and Translational Cancer Biology Program, Biomedicum Helsinki, 00014 University of Helsinki, Finland, 2Program in Developmental Biology, Institute of Biotechnology, University of Helsinki, P.O. Box 56, Viikinkaari 5D, 00014, Helsinki, , Finland, 3Inserm U970, Paris Cardiovascular Research Center, Paris 75015, , France, 4Department of Neurology, Yale University School of Medicine, New Haven, Connecticut 06520, , USA, 5Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06511, , USA, 6Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, , USA, 7Sorbonne Universités, UPMC Univ Paris 06, Inserm U1127, CNRS, AP-HP, Institut du Cerveau et de la Moelle Epinière (ICM), Hôpital Pitié-Salpêtrière, Boulevard de l’Hôpital, F-75013, Paris, , France

• Meningeal lymphatic network develops postna-tally

• VEGF-C and VEGFR3 are essential for develop-ment and maintenance of meningeal lymphatic vessels

• Meningeal lymphatic vessels and their function can be modulated with VEGF-C/VEGFR3 pathway also at adult age

Posters – Monday

– 32 –

IVBM2018

M016

Inhibition of endothelial PMCA4 as a novel pro-angiogenic therapy for ischaemic cardio-vascular disease

Sathishkumar Kurusamy1, Dolores Lopez-Maderuelo2,3, Robert Little4, David Cadagan1, Aaron M Savage5, Jude C Ihugba1, Rhiannon R Baggott1, Farjana B Rowther6, Sara Martinez-Martinez2,3, Pablo Gomez-Del Arco2,3,7, Miss Clare Murcott1, Weiguang Wang8, Delvac Oceandy4, Ludwig Neyses4,9, Robert N Wilkinson5, Elizabeth J Cartwright4, Juan Miguel Redondo2,3, Angel L Armesilla1,3

1Cardiovascular Molecular Pharmacology laboratory, RIHS, School of Pharmacy, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton, United Kingdom, 2Gene Regulation in Cardiovascular Remodelling and Inflammation Group, Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain, 3CIBERCV, , Spain, 4Division of Cardiovascular Sciences, Manchester Academic Health Science Centre, University of Manchester, Manchester, United Kingdom, 5Department of Infection, Immunity & Cardiovascular disease & Bateson Centre, University of Sheffield, Sheffield, United Kingdom, 6Brain Tumor UK NeuroOncology Research Centre, RIHS, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton, United Kingdom, 7Department of Molecular Biology, Universidad Autonoma de Madrid (CBM-SO), Madrid, Spain, 8Oncology Laboratory, RIHS, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton, United Kingdom, 9University of Luxembourg, , Luxembourg

• Endothelial Plasma Membrane Calcium ATPase 4 (PMCA4) negatively regulates VEGF-driven angio-genesis via interaction with the signalling protein calcineurin.

• Inhibition of PMCA4 activity in endothelial cells using nanomolar concentrations of the small molecule aurintricarboxylic acid enhances calci-neurin signalling and VEGF-induced angiogenesis.

• 3. Selective inhibition of PMCA4 in endothe-lial cells might be used to improve VEGF-based pro-angiogenic therapeutic interventions.

M017

Loss of Vezf1 impairs β-adrenergic stimuli -induced cardiac growth and contractile func-tion

Jere Paavola1,3, Johanna Ulvila2, Tarja Alakoski2, Teemu Kilpiö2,4, Juuso Sirén1, Sanni Perttunen1, Päivi Lakkisto1,5, Ilkka Tikkanen1,6, Risto Kerkelä2,4

1Unit of Cardiovascular Research, Minerva Institute for Medical Research, Biomedicum Helsinki, Helsinki, Finland, 2Research Unit of Biomedicine, University of Oulu, Oulu, Finland, 3Internal Medicine, Jorvi Hospital, Helsinki University Hospital, Espoo, Finland, 4Medical Research Centre Oulu, Oulu University Hospital and University of Oulu, Oulu, Finland, 5Clinical Chemistry and Hematology, Helsinki University Hospital, Helsinki, Finland, 6Abdominal Center, Nephrology, Helsinki University Hospital, Helsinki, Finland

• Expression of Vezf1 in the heart is downregulated in human cardiomyopathies

• Zebrafish Vezf1 is necessary for hemodynamic stress –induced cardiac growth and cardiac con-tractile response, and loss of Vezf1 results in greater propensity towards heart failure.

• Molecular analysis for Vezf1 function in cardio-myocytes identifies an MCAT binding site as tar-get for Vezf1.

M018

Extracorporeal application of eddy brakes to control magnetic nanoparticles and modulat-ing the drift and diffusion

Mark Christopher Arokiaraj1

1Pondicherry Institute Of Medical Sciences, Pondicherry, India

• It is feasible to control the movement of magnetic nanoparticles in the heart using eddy breaks by extracorporeal method.

• Also, the diffusion and drift characteristics of the multifunctional nanoparticles can be modulated.

• Using this ischemia/hypoxic salvage, targeted angiogenesis, modification of endothelial func-tions and changes in cardiac extracellular matrix is feasible.

Posters – Monday

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IVBM2018

M019

Apoproteins modulate tumor angiogenesis and metastasis formation via differential regu-lation of VEGF receptors

Lihee Asaf1, Yogev Sela1, Ifah Raviv1, Yona Eli1, Ehud Zigmond2, Chen Varol2, Karina Yaniv1

1Weizmann Institute Of Science, Rehovot, Israel, 2Research Center for Digestive Tract & Liver Diseases, Sourasky Medical Center, Tel Aviv, Israel

• Lipoprotein levels are inversely correlated with tumor vascularization in LDLR and ApoE KO mice. We uncovered a deleterious role for ApoB100 and ApoE as direct inhibitors of tumor vascular-ization.

• VEGF receptors are downstream targets of apoproteins within endothelial cells, and their endothelial-specific ablation in vivo rescues the anti-angiogenic phenotype.

M020

Collateral and capillary rarefaction is asso-ciated with reduced alternative macrophage activation in type 2 diabetes

Mohan Babu1, Durga Devi Thota1, Minna Kaikkonen1, Petri Mäkinen1, Hanne Laakso1, Timo Liimatainen1, Seppo Ylä-Herttuala1

1Dept of Biotechnology and Molecular Medicine, Aiv Institute, University of Eastern Finland, Kuopio, Finland

• Collateral rarefaction in diabetic muscles is asso-ciated with reduced alternative macrophage acti-vation.

• Diabetic mice display reduced vascularity ratio and increased tissue damage in response to limb ischemia.

• Impaired angiogenesis, reduced endothelial tip cells and endothelial cell proliferation in ischemic muscles is associated with reduced alternative macrophage activation.

M021

MicroRNA-34a promotes senescence-medi-ated vascular smooth muscle cells calcifica-tion by downregulating SIRT1 and Axl

Ileana Badi1, Luigi Mancinelli1, Debora Ferri1, Andrea Polizzotto1, Filippo Zeni1, Ilaria Burba1, Francesca Brambilla2, Claudio Saccu1, Marco E. Bianchi2, Giulio Pompilio1, Maurizio C. Capogrossi3, Angela Raucci1

1Centro Cardiologico Monzino, Milan, Italy, 2IRCCS San Raffaele Scientific Institute, Milan, Italy, 3Ochsner Medical Center, New Orleans, USA

• Mir34a genetic ablation reduces soft tissue and vascular calcification.

• miR-34a promotes vascular smooth muscle cell calcification by inducing cell growth arrest and senescence.

• miR-34a affects the expression of targets, such as Axl and SIRT1, that are vascular calcification inhibitors.

M022

Human IgG1 phosphorylcholine antibody reduces vein graft remodeling, intraplaque angiogenesis, and intraplaque hemorrhage

Fabiana Baganha1,2, Margreet de Vries1,2, Erna Peters1,2, Knut Pettersson3, Paul Quax11,2

1Leiden University Medical Center, Leiden, Netherlands, 2Einthoven Laboratory for Experimental Vascular Medicine, Leiden, Netherlands, 3Athera Biotechnologies, Mölndal, Sweden

• Low levels of natural IgM phosphorylcholine anti-bodies are associated with increased risk for car-diovascular events.

• Intraplaque neovessels are immature resulting in the leakage of circulating cells - intraplaque hemorrhage - leading to an increased cholesterol deposition, atheroma growth, and plaque insta-bility.

• PCmAb, a humanized IgG1 phosphorylcholine antibody, is an effective inhibitor of intraplaque angiogenesis and intraplaque hemorrhage.

Posters – Monday

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IVBM2018

M024

Loss of BMP9 protects against experimental pulmonary arterial hypertension

Ly Tu1,2, Christine Mallet3,4,5, Ayumi Sekine1,2, Jennifer Bordenave1,2, Agnès Desroches-Castan3,4,5, Raphaël Thuillet1,2, Carole Phan1,2, Florian Robert3,4,5, Paul-Benoit Poble1,2, Alice Huertas1,2, Pr Marc Humbert1,2, Christophe Guignabert1,2, Sabine Bailly3,4,5

1INSERM UMR_999, Le plessis Robinson, France, 2Université Paris-Sud, Université Paris-Saclay, Kremlin-Bicêtre, France, 3U1036, Grenoble, France, 4Univ. Grenoble Alpes, Grenoble, France, 5BIG-Biologie du Cancer et de l’Infection CEA, Grenoble, France

• Heterozygous germline mutations in the BMPR2 gene and more rarely in the ACVRL1 gene have been identified as critical genetic factors predis-posing to PAH.

• The loss of BMP9, by deletion or inhibition, pro-tects rodents against the development of exper-imental PAH.

• BMP9 regulates several factors implicated in the regulation of vascular tone (endothelin-1, apelin and adrenomedullin) that could explain these results.

M025

Integrity of the blood-brain and blood-cere-brospinal fluid barrier in spontaneously hyper-tensive rats

Daphne M. Naessens1, Judith de Vos1, Ed VanBavel1, Erik N.T.P. Bakker1

1AMC, Amsterdam, Nederland

• Hypertension is an important risk factor for cere-brovascular disease, including stroke and vascular dementia

• We hypothesized that cerebrovascular damage would manifest itself in leakage of the blood-brain barrier (BBB) and blood-cerebrospinal fluid barrier (BCSFB).

• 3. Surprisingly, we found no evidence for BBB or BCSFB dysfunction in spontaneously hypertensive rat at 10 months of age.

M026

Lymph Flow Mediated Postnatal Remodel-ing of Meningeal Lymphatics Coincides with Beginning of Drainage of Macromolecules

Laszlo Balint1,2, Zsombor Ocskay1,2, Balint Andras Deak1,2, Zoltan Jakus1,2

11, Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary, 22, MTA-SE „Lendület” Lymphatic Physiology Research Group of the Hungarian Academy of Sciences and the Semmelweis University, Budapest, Hungary

• Meningeal lymphatics present in the dura mater are involved in the uptake and transport of mac-romolecules injected into the CNS

• A lymph flow mediated structural remodeling of meningeal lymphatics occurs during the postna-tal period

• Lymph flow mediated postnatal remodeling of meningeal lymphatics coincides with the begin-ning of the drainage of macromolecules from the CNS

M027

EphrinB2/EphB4 signaling regulates non-sprouting angiogenesis by VEGF

Elena Groppa1, Sime Brkic1, Andrea Uccelli1, Galina Wirth2, Petra Korpisalo-Pirinen2, Maria Filippova1, Boris Dasen1, Veronica Sacchi1, Manuele Muraro1, Marianna Trani1, Silvia Reginato1, Roberto Gianni-Barrera1, Seppo Ylä-Herttuala2,3, Dr Andrea Banfi1

1Department of Biomedicine, Basel University Hospital, Basel, Switzerland, 2A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland, 3Heart Center, Kuopio University Hospital, Kuopio, Finland

• Therapeutic VEGF delivery to ischemic muscle induces angiogenesis by intussusception (vascu-lar splitting) rather than sprouting

• EphB4 finely tunes the degree of endothelial pro-liferation by specific VEGF doses in vivo, regulat-ing VEGF-R2 signaling output through p-ERK1/2

• Pharmacologic EphB4 stimulation limits the size of initial vessel enlargement, enabling splitting into normal capillaries, and ensures exclusively physiological angiogenesis

Posters – Monday

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IVBM2018

M028

Similarities and differences in the pathology of thoracic aortic aneurysm and the mega-aortic syndrome

Ulrike Baranyi1, Christian Stern1,2, Birgitta Winter1, Adrian Türkcan1,3, Bernhard Scharinger1,3, Marie Teres Stelzmüller6, Thomas Aschacher6, Ass. Martin Andreas6, Ao. Marek Ehrlich6, Günther Laufer6, Ass. David Bernhard4,5, Assoc. Barbara Messner1

1Medical University of Vienna,Department of Surgery, Cardiac Surgery Laboratory, Vienna, Austria, 2Medical Faculty of the Martin Luther University Halle (Saale), Halle , Germany, 3Ludwig Maximilian University Munich, Munich, Germany, 4Innsbruck Medical University,Cardiac Surgery Research Laboratory Innsbruck, Innsbruck, Austria, 5Johannes Kepler University Linz, Center for Medical Research, Linz, Austria, 6Medical University of Vienna, Department of Cardiac Surgery, Vienna, Austria

• Tissues of patients with Thoracic aortic aneu-rysm (TAA) with different luminal size and the mega-aortic syndrome (MAS) were investigated.

• Specimens of the MAS are related to atheroscle-rosis in the ascending aorta compared to speci-mens of TAA tissue.

• Infiltrations of CD68+ macrophages were signifi-cantly elevated in TAA samples and are the main producers of MMP9.

M029

Novel mechanisms underlying the formation of the Blood-Brain Barrier

Ivan Bassi1, Gideon Hen1, Moshe Grunspan1, Karina Yaniv1

1Weizmann Institute Of Science, Rehovot, Israel

• weakyleak mutant fish display morphological defects in the cerebral vasculature, massive hem-orrhage and bloated lysosomes.

• notch and glut1 downregulation suggest a role for scarb2 in the early stage of BBB development

• weakyleak mutant represent the first in vivo model to investigate the link between lysosome storage disease and BBB breakdown.

M030

Microtubule dynamics in vessel morphogene-sis and homeostasis

Marta Bastos de Oliveira1, Russil Collins1, Holger Gerhardt1,2,3,4

1Max Delbrück Center, Berlin, Germany, 2Vesalius Research Center, VIB, KU Leuven, Leuven, Belgium, 3DZHK (German Center for Cardiovascular Research), Berlin , Germany, 4Berlin Institute of Health , Berlin, Germany

• Cancer patients treated with drugs which interfere with microtubule dynamics exhibit a decrease in tumour vascularisation, which helps their recovery.

• Microtubule growth rate is faster in endothelial cells undergoing angiogenesis than in matured ones.

• Microtubules’ dynamics are necessary for angio-genesis, but not for the maintenance of already formed vessel networks.

M031

Hang on and move – junctional dynamics during vascular morphogenesis

Ilkka Paatero1,3, Loïc Sauteur1, Minkyoung Lee1, Anne K. Lagendijk3, Daniel Heutschi1, Cora Wiesner1, Camilo Gúzman3, Dimitri Bieli Bieli1, Benjamin M. Hogan2, Markus Affolter1, Heinz-Georg Belting1

1Biozentrum/University Of Basel, Basel, Switzerland, 2IMB, University of Queensland, St Lucia, Australia, 3Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

• We have analyzed dynamics and function of junc-tional components during vascular remodeling in vivo.

• Morphogenetic EC behaviors are driven by polar-ized and oscillating junction-based lamellipodia (JBL).

• JBL function as ratchet via VE-cad/F-actin interac-tion and provide the physical means for cell rear-rangements.

Posters – Monday

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IVBM2018

M032

Extracellular vesicle and plaque microRNA-155 expression is dysregulated in human atherosclerotic disease progression

Stephen Ftizsimons1, Niall Mahon2, Nicola Ryan2, Stehpen Sheehan3, Mary Barry3, Orina Belton1

1Diabetic Complications Research Centre, School of Biomolecular and Biomedical Sciences University College Dublin, Dublin, Ireland, 2Mater Misericordiae University Hospital, Dublin, Ireland, 3St Vincent’s University Hospital, Dublin, Ireland

• Extracellular vesicles (EVs) facilitate cell-to-cell communication and have potential as diagnostic and prognostic biomarkers

• Our data shows that as atherosclerosis pro-gresses there is a decrease in urinary EV con-centration coincident with an increase in both urinary EV and human atherosclerotic plaque miR-155 expression.

• Urinary EV miR-155 expression reflects athero-sclerotic plaque progression and may represent a novel prognostic tool.

M033

Optimizing intra-islet blood vessel formation to enhance an ex vivo Islet-on-a-Chip plat-form

R. Hugh F. Bender1, Matthew Wortham2,3, Bhupinder Shergill6, Kim-Vy Nguyen-Ngoc2,3, Roberto Gaetani5, Karen L. Christman3,5, Steven C. George6, Maike Sander2,3,4, Christopher C.W. Hughes1

1Dept. of Molecular Biology & Biochemistry, University Of California, Irvine, Irvine, United States, 2Pediatric Diabetes Research Center, Dept. of Pediatrics, University of California, San Diego, San Diego, USA, 3Sanford Consortium for Regenerative Medicine, University of California, San Diego, San Diego, USA, 4Dept. of Cellular & Molecular Medicine, University of California, San Diego, San Diego, USA, 5Dept. of Bioengineering, University of California, San Diego, San Diego, USA, 6Dept. of Biomedical Engineering, University of California, Davis, Davis, USA

• Studies on β cell dysfunction in diabetes have his-torically relied on in vitro techniques that fail to maintain islet functionality.

• Our 3D, vascularized, Islet-on-a-Chip platform facilitates functional human islet maintenance for up to two weeks ex vivo.

• We have recently optimized methods for gener-ating islets that form intra-islet vasculature, a key hallmark of islets in vivo.

M034

Genetic Deletion of Telomerase Predisposes for Doxorubicin-Induced Microvascular Dys-function Preceding Development of Heart Failure

Jasmine Linn1,2, Dana Murphy1,2, Matt Hoffman2,3, Laura Norwood Toro1,2, Michael Flister2,3, Andreas M. Beyer1,2,3,4

1Department of Medicine Medical College Of Wisconsin, MIlwaukee , United States, 2Department of Physiology Medical College Of Wisconsin, MIlwaukee , United States, 3Cardiovascular center Medical College Of Wisconsin, Milwaukee, United States, 4Redox Biology Program Medical College Of Wisconsin, Milwaukee, United States

• TERT KO rats show signs of decreased diastolic heart function

• TERT KO rats have elevated systemic blood pres-sure

• TERT KO rats develop microvascular dysfunction before onset of chemotherapy-induced heart fail-ure

M035

Investigating the role of endothelial cell mor-phology in nitric oxide production

Aparna Bhattacharyya1, Kenneth Barbee1

1Drexel University, Philadelphia, United States

• Basal eNOS phosphorylation is similar in elon-gated and aligned BAECs and those that are polygonal and randomly oriented.

• ATP, VEGF and bradykinin induce eNOS phosphor-ylation to a greater extent in elongated cells than in polygonal cells.

• Endothelial cell elongation is correlated with increased sensitivity to agonists that modulate eNOS activity

Posters – Monday

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IVBM2018

M036

Cellular and Biomimicking In Vitro Models to Study Capillary Malformations

Colette Bichsel1,2, Lan Huang1,2, Sanda Alexandrescu3, Anna Pinto4, Joyce Bischoff1,2

1Vascular Biology Program, Boston Children’s Hospital and Harvard Medical School, Boston, United States, 2Department of Surgery, Boston Children’s Hospital , Boston, United States, 3Department of Pathology, Boston Children’s Hospital, Boston, United States, 4Department of Neurology, Boston Children’s Hospital, Boston, United States

• Capillary malformations (CM) are caused by somatic mutation in GNAQ in endothelial cells and are associated with novel perivascular acces-sory cells.

• CRISPR/Cas9 was used to introduce the GNAQ point mutation into primary human endothelial cells.

• GNAQ-mutant endothelial cells show decreased proliferation but form vessels with accessory cells in a 3D in vitro microvascular model.

M037

TNIP2: a novel regulator of inflammatory lymphangiogenesis in human atherosclerosis

Marchy Kietadisorn1, Marco Manca1, Timo Rademakers1, Frank Ruehle2, Monica Stoll1,2, Franck Dequiedt3, Judith Sluimer1, Àgnes Noel3, Erik Biessen1

1University Maastricht, Maastricht, Netherlands, 2University of Muenster, Muenster, Germany, 3University of Liege, Liege, Belgium

• advanced atherosclerosis is typified by major expansion of the lymphactic bed.

• genomics analysis unveils a gene program cor-relating with plaque lymphatics.

• TNIP2 is identified as novel regulator of plaque lymphangiogenesis.

M038

New Insights into PRL2 function in angiogen-esis and arteriovenous differentiation

Mathilde Poulet1,2,3, Jacinth Sirois3, Tiffanie Chouleur1,2,3, Kevin Boye1,2, Serge Hardy3, Thomas Daubon1,2, Noriko Uetani3, Michel Tremblay3, Andreas Bikfalvi1,2

1Inserm U1029, Pessac, France, 2University Bordeaux, Pessac, France, 3Goodman Cancer Centre - Mc Gill University, Montreal, Canada

• PRL2 is a regulator of vascular development,• PRL2 modulates VEGF and Notch signalling,• PRL2 is involved in arterio-venous differentiation

M039

The role of the long non-coding LINC-PINT in endothelial function

Diewertje Bink1, Patrick Hofmann2, Noelia Lozano Vidal1, Hanjoong Jo3, Stefanie Dimmeler2, Jolanda van der Velden1,4, Reinier Boon1,2

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands, 2Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, Frankfurt, Germany, 3Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Atlanta, USA, 4ICIN- Netherlands Heart Institute, Utrecht, the Netherlands

• The long non-coding RNA LINC-PINT is upreg-ulated with age in mouse tissue and primary human endothelial cell lines.

• Knockdown of LINC-PINT with LNA GapmeRs increases apoptosis and reduces proliferation, migration and sprouting in HUVECs.

• LINC-PINT binds to EZH2 and thereby influences gene transcription of P21, ICAM1, VCAM1 and VEGF, affecting endothelial cell function.

M040

The role of long non-coding RNA TERRA in endothelial function

Diewertje Bink1, Patrick Hofmann2, Stefanie Dimmeler2, Jolanda van der Velden1,3, Reinier Boon1,2

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, the Netherlands, 2Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany, 3ICIN- Netherlands Heart Institute, Utrecht, the Netherlands

• Long non-coding RNA transcripts called Telomeric repeat-containing RNA (TERRA) are transcribed from the subtelomeres and telomeres of most chromosomes.

• TERRA molecules from different chromosomes are upregulated with age in mouse tissue and pri-mary human endothelial cell lines.

• H20q-TERRA knockdown with LNA GapmeRs shortens telomere length, increases apoptosis and reduces sprouting in HUVECs, affecting endo-thelial cell function.

Posters – Monday

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IVBM2018

M041

The ETS factor ERG controls an endotheli-al-specific transcriptional regulatory program associated with super-enhancers

Viktoria Kalna1, Youwen Yang1, Claire R. Peghaire1, Rebecca Hannah2, Aarti V. Shah1, Lourdes Osuna Almagro1, Joseph J. Boyle1, Jorge Ferrer1, Berthold Gottgens2, Anna M. Randi1, Graeme M. Birdsey1

1Imperial College London, London, United Kingdom, 2University of Cambridge, Cambridge, United Kingdom

• ERG is essential for endothelial lineage specifi-cation, driving expression of genes such as VWF, CDH5, DLL4, and CLDN5.

• ERG dynamically modulates endothelial enhancers and super-enhancers associated with changes in gene expression.

• ERG is a lineage-determining transcription factor that regulates cell type-specific super-enhancer profiles.

M042

TGF-β regulation of outflow tract development and function in zebrafish

Giulia LM Boezio1, Anabela Bensimon-Brito1, Didier YR Stainier1, Christian SM Helker1

1Max Planck Institute For Heart And Lung Research, Bad Nauheim, Germany

• TgfbrI is expressed in the zebrafish heart (ventri-cle and outflow tract) during larval development.

• CRISPR/Cas9 mutations in TgfbrI lead to a dilation of the heart outflow tract and malformations of the ventral artery.

• The outflow tract dilation in TgfbrI mutant larvae resembles the ascending artery’s defects in TAAD human patients.

M043

Transdifferentiation of human fibroblasts to smooth muscle cells for the study of aortic aneurysm pathology

Natalija Bogunovic1, Dimitra Micha1, Willem Wisselink1, Jan D. Blankensteijn1, Kak K. Yeung1

1Vumc, Amsterdam, Netherlands

• Direct conversion of one mature cell type into another using a growth factor and a specific scaf-fold within fourteen days

• Characterization of smooth muscle cell specific markers on mRNA and protein level, confirming the transdifferentiation into smooth muscle cells

• Application of the method to study pathogenic variants in smooth muscle cell genes causing aor-tic aneurysms

M044

RBMS1: through the eye of angiogenesis.

Rebecca Bolton1, James Brash1, Christiana Ruhrberg1

1Ucl , London, United Kingdom

• RBMS1 is a nucleic acid-binding protein and a candidate effector of NRP1, a transmembrane receptor with roles in developmental angiogene-sis.

• RBMS1-deletion is embryonic lethal, and endo-thelial cell (EC)-specific deletion of RBMS1 causes defective angiogenesis in the postnatal retina.

• ECs lacking RBMS1 have reduced expression of EC markers and increased expression of mesen-chymal markers, indicative of endothelial-to-mes-enchymal transition.

Posters – Monday

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IVBM2018

M045

Desmoglein-2, an unsuspected regulator of tumour vasculature and immune response in melanoma.

Claudine Bonder1, Lih Tan1, Kay Khine Myo Min1, Michaelia Cockshell1, Jeff Holst2, Michael Brown1, Mark Shackleton3, Lisa Ebert1

1Centre for Cancer Biology, Adelaide, Australia, 2Centenary Institute and the University of Sydney, Sydney, Australia, 3Alfred Health and Monash University, Melbourne, Australia

• tumour growth and metastasis requires access to a blood supply

• desmoglein-2 is a cadherin adhesion molecule that is pro-angiogenic and promotes vasculogenic mimicry in melanoma

• inhibition of desmoglein-2 perturbs cancer growth in vivo by changing the immune response

M046

ABL kinase inhibitor Ponatinib combined with rapamycin causes regression of murine Venous Malformation

Xian Li1, Yuqi Cai1, Jillian Goines1, Elisa Boscolo1

1Cincinnati Children’s Hospital, Cincinnati, United States

• screening for candidate drugs targeting mutant-TIE2 signaling in venous malformation (VM)

• Ponatinib affects TIE2 and cABL activity down-stream of mutant TIE2

• Ponatinib combined with rapamycin induces regression of mutated-TIE2 derived murinemodel of VM

M047

Hypercholesterolemia promotes a mast cell-CD4+ T-cell interaction in atherosclerosis

Ilze Bot1, Eva Kritikou1, Thomas van der Heijden1, Maarten Swart1, Janine van Duijn1, Bram Slütter1, Harm Smeets2, Anouk Wezel2, Pasquale Maffia3, Johan Kuiper1

1LACDR/Leiden University, Leiden, Netherlands, 2HMC Westeinde, Den Haag, Netherlands, 3Centre for Immunobiology, Institute of Infection, Glasgow, UK

• Upon hyperlipidemia mast cells increase their MHCII expression, present antigens and promote T cell proliferation.

• Human atherosclerotic plaque mast cells express MHCII, suggesting that mast cells may be capable of antigen presentation inside the human athero-sclerotic plaque.

• Mast cells may function as non-classical antigen presenting cells in atherosclerosis.

M048

Preventive effect of Indirubin-3 monoxime on cerebral cavernous malformations (CCM).

Gwénola Boulday1, Cécile Otten2, Mathias Eymery3, Cécile Cardoso1, Coralie De-Luca1, Minh Arnould1, Corinne Albiges-Rizo3, Eva Faurobert3, Salim Abdelilah-Seyfried2, Elisabeth Tournier-Lasserve1,4

1INSERM UMR-1161, Université Paris Diderot, Génétique et physiopathologie des maladies cérébro-vasculaires, Paris, France, 2Institute of Biochemistry and Biology, Potsdam University, Potsdam, Germany, 3INSERM U1209, Université Grenoble Alpes, Institute for Advanced Biosciences, France, 4AP-HP, Groupe hospitalier Saint-Louis, Lariboisière, Fernand-Widal, Service de génétique moléculaire neuro-vasculaire, Paris, France

• IR3mo suppresses CCM phenotype in CCM1-de-pleted HUVEC and CCM2 zebrafish mutant

• IR3mo prevents cerebrovascular lesion develop-ment in both CCM2 and CCM3 mouse models

• IR3mo prevents Klf2 enhanced expression and MAPK activation upon CCM loss in vitro

M049

TGFβ signaling via ALK1 and ALK5 regulates distinct functional pathways in vein graft inti-mal hyperplasia

Emma Low1, Julian Schwartze1, Daniel Kelly1, Sammy El-Mansi1, Andrew Shaw1, Midori Thorikay2, John McClure1, Martin McBride1, Nick Morrell3, Peter ten Dijke2, Andy Baker4, Angela Bradshaw1

1University Of Glasgow, Glasgow, United Kingdom, 2University of Edinburgh, Edinburgh, United Kingdom, 3Leiden University Medical Centre, Leiden, Holland, 4University of Cambridge, Cambridge, United Kingdom

• TGFβ activates Smad1/5 via ALK1 in SMCs from hyperplastic saphenous vein grafts

• TGFβ signaling via ALK1 in SMCs regulates distinct behavioural responses and transcriptional path-ways to ALK5/TβRI

• Smad1/5 activation is a hallmark of the SMC response to acute vascular injury; knockout or pharmacological inhibition of pSmad1/5 attenu-ates neointima formation in vivo

Posters – Monday

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IVBM2018

M050

Tollip controls atherogenesis through regula-tion of autophagy-mediated degradation of low-density lipoprotein receptor.

Karim Brandt1, Daniela Baptista1, Aline Roth1, Fabienne Burger1, Rodrigo Fraga-Silva2, Nicolas Stergiopulos2, François Mach1

1University Of Geneva, Geneva, Switzerland, 2Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland

• Tollip is atheroprotective• Tollip controls posttranscriptional expression of

LDLR• Tollip controls LDLR autophagy-mediated degra-

dation

M051

The Cdc42-GEF FGD5 is necessary to main-tain integrity of challenged endothelial con-tacts.

Laura Braun1, Maren Holm1, Kerstin Schäfer1, Kevin Peters2, Dietmar Vestweber1

1Max Planck Institute For Molecular Biomedicine, Münster, Germany, 2Aerpio Pharmaceuticals, Cincinnati, USA

• FGD5 is a target of VE-PTP.• Pharmacological VE-PTP inhibition induces the

activation of FGD5.• FGD5 expression is necessary for endothelial con-

tact stability during inflammation.

M052

Single-cell transcriptomics of lymphoid tissue blood endothelial cells

Kevin Brulois1, Agata Szade1, Anusha Rajaraman1, Eugene Butcher1

1Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford School of Medicine, Stanford, United States

• A single-cell survey blood endothelium from mouse and and human lymphoid tissues

• Identification of novel subsets and development relationships

• Integrated and analysis of mouse and human datasets

M053

Insulin-like growth factor binding protein 2 (IGFBP2) positively regulates angiogenesis

Alexander-Francisco Bruns1, Jessica Smith1, Nadira Yuldasheva1, Mark T. Kearney1, Stephen B. Wheatcroft1

1LICAMM / University Of Leeds, Leeds, United Kingdom

• IGFBP2 activated MAPK via β1 integrin.• IGFBP2 increased the number of cellular protru-

sions in a three dimensional culture assay.• Global, constitutive overexpression of human

IGFBP2 in mice increased tip cell formation in the postnatal retina.

M054

Factor VII Activating Protease (FSAP) medi-ates cellular responses through Protease Acti-vated Receptors (PARs).

Kristina Byskov1, Thomas Boettger2, Sylvain Le Gall3, Paul F. Ruehle4, Nis Valentin Nielsen1, Bernd Thiede5, Michael Etscheid6, Eric Camerer3, Sandip M. Kanse1,7

1Institute of Basic Medical Sciences, University of Oslo, Oslo, Norway, 2Max Planck Institute, Bad Nauheim, Germany, 3Inserm U970, Paris Cardiovascular Research Centre, Paris, France, 4Department of Radiation Oncology, Universitaetsklinikum Erlangen, Erlangen-Nuerenberg, Germany, 5Department of Biosciences, Faculty of Mathematics and Natural Sciences, University of Oslo, Oslo, Norway, 6Paul Ehrlich Institute , Langen, Germany, 7Oslo University Hospital, Oslo, Norway

• FSAP, a circulating serine protease, is a novel mediator in hemostasis and vascular biology.

• FSAP cleaves PAR-1 and PAR2 at canonical cleav-age sites and activates cellular signaling.

• FSAP induces expression of genes related to pro-liferation, apoptosis and inflammation in VSMC in a PAR-1-dependent manner.

Posters – Monday

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IVBM2018

M055

IL-7-dependent chemokine production by intestinal endothelial cells during acute HIV/SIV infection.

Carolina Cabe1, Magali Rancez1, Bénédicte de Muylder1, Suzanne Morgado1, Magali Mas1, Rémi Cheynier1, Anne Couedel- Courteille1,2

1Institut Cochin - INSERM U1016 - CNRS UMR8104 - Université Paris Descartes, Sorbonne Paris Cité, Paris, France, 2Université Paris Diderot, Paris, France

• Increased CD127 expression by endothelial cells upon stimulation by inflammatory cytokines with higher expression when IL-7 is added.

• In combination with inflammatory cytokines, IL-7 triggers chemokine expression by endothelial cells, leading to mucosal immune cell homing.

• In response to IL-7, endothelial cells participate to the establishment of the immune response to acute infection.

M056

QKI-6 induced VSMC differentiation from pluripotent stem cells by facilitating HDAC7 splicing

Rachel Caines1, Amy Cochrane1, Marta Vilà-González1, Sophia Kelaini1, Marianna Tsifaki1, Chunbo Yang1, Alan Stitt1, David Grieve1, Lingfang Zeng2, Andriana Margariti1

1The Wellcome-Wolfson Building, Centre for Experimental Medicine, Queen’s University Belfast, BT9 7BL, , United Kingdom, 2Cardiovascular Division, King’s College London, SE5 9NU, , United Kingdom

• QKI-6 was identified as a novel regulator of Vas-cular Smooth Muscle Cell differentiation from mouse induced pluripotent stem cells

• QKI-6 can bind to HDAC7 intron 1, regulating HDAC7 splicing, inducing vascular smooth muscle cell differentiation

• Elucidating pathways of vascular smooth muscle cell differentiation through iPS technology could lead to the discovery of new therapeutic targets

M057

Non-muscle-myosin-II heavy chain isoforms distinctly control endothelial junction dynam-ics, permeability, and cell migration

Jiahui Cao1, Matthias Brandt2, Timo Betz2, Hans Schnittler1

1Institute of Anatomy and Vascular Biology, Univeristy of Munester, Muenster, Germany, 2Institute of Cell Biology, ZMBE, University of Muenster , Muenster, Germany

• The balance level of NMIIA and NMIIB deter-mine stress fiber assembly, while only NMIIA is recruited and terminated lamellipodia

• NMIIA and NMIIB has contrary role to control endothelial junction dynamics and barrier func-tion

• Both NMIIA and NMIIB are required for cell migration and in vitro angiogenesis

M058

Impact of circadian rhythm in smooth muscle cells.

Luis Miguel Cardoso dos Santos1, Laurent Perrin2, Matteo Coen3, Marie-Luce Bochaton-Piallat1, Charna Dibner2

1Dept of Pathology and Immunology, Faculty of Medicine, University of Geneva, Geneva, Switzerland, 2Dept of Cell Physiology and Metabolism, Faculty of Medicine, University of Geneva, Geneva, Switzerland, 3Service of Internal Medicine, Geneva University Hospitals , Geneva, Switzerland

• Spindle-shaped (S) and rhomboid (R) smooth muscle cells isolated from the porcine coronary artery correspond to the contractile and syn-thetic phenotype, respectively.

• They exhibit distinct circadian profiles for several core clock genes, as shown through biolumines-cence assays and qPCR.

• Our results suggest a possible link between circa-dian oscillators operative in SMCs and regulators of SMC plasticity.

Posters – Monday

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IVBM2018

M059

Tie-1 signaling in zebrafish cardiovascular development

Claudia Carlantoni1, Zacharias Kontarakis1, Andrea Rossi1, Didier Y.R. Stainier1


• Our CRISPR zebrafish tie-1Δ7 mutants show a dramatic reduction in tie-1 transcript levels.

• Mutant embryos display reduced common car-dinal vein (CCV) width and detachment between endocardium and myocardium.

• Endothelial/endocardial cell number is signifi-cantly reduced in tie-1Δ7 mutants, possibly linked to proliferation, survival and/or migration defects.

M060

The G-protein coupled receptor ChemR23 determines smooth muscle cell phenotypic switching and alters vascular calcification

Miguel Carracedo Ortiz1, Gonzalo Artiach1, Anna Witasp2, Joan Claria3, Mattias Carlström4, Andrés Laguna-Fernandez1, Magnus Bäck1,5

1Department of Medicine Solna Karolinska Institutet, Solna, Sweden, 2Division of Renal Medicine, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden, 3Department of Biochemistry and Molecular Genetics, Hospital Clínic-IDIBAPS and Department of Biomedical Sciences University of Barcelona, Barcelona, Spain, 4Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden, 5Theme Heart and Vessels, Divison of Valvular and Coronary Disease, Karolinska University Hospital, Stockholm, Sweden

• ChemR23 deficiency preserves a contractile SMC phenotype and protects from vascular calcifica-tion in vitro and in vivo

• RvE1 inhibits calcification through ChemR23• ChemR23 is an inducer of VSMC phenotypic

switch into a synthetic and osteoblastic pheno-type favoring vascular calcification

M061

TRAIL expressing monocyte/macrophages are critical for the prevention of inflammation and atherosclerosis.

Sian Cartland1,2, Scott Genner1, Gonzalo Martinez2,3,4, Stacy Robertson1,2, Maaike Kockx5, John O’Sullivan1,2,3, Yen Chin Koay1,2, Pradeep Manuneedhi Cholan1,2, Andrew Murphy6, Martin Bennett7, Wendy Jessup5, Leonard Kritharides5,8, Carolyn Geczy1,9, Sanjay Patel1,2,3, Mary Kavurma1,2

1Heart Research Institute, Sydney, Australia, 2University of Sydney, Sydney, Australia, 3Royal Prince Alfred Hospital, Sydney, Australia, 4Division of Cardiovascular Diseases, Pontificia Universidad Católica, Santiago, Chile, 5ANZAC Research Institute, Sydney, Australia, 6Baker IDI, Melbourne, Australia, 7Division of Cardiovascular Medicine, University of Cambridge, Cambridge, United Kingdom, 8Department of Cardiology, Concord Repatriation General Hospital, Sydney, Australia, 9School of Medical Sciences, University of New South Wales, Sydney, Australia

• TRAIL expression is significantly reduced in mono-cytes from coronary artery disease patients, con-comitant with circulating levels of TRAIL.

• iNOShi TRAIL+ macrophages are important in the resolution of atherosclerosis in mice

• Macrophages lacking TRAIL are more inflamma-tory, and have impaired functions that contribute to increased foam cells in lesions

M062

Opposing effects on VSMC proliferation and inflammation reveal protective role for ChemR23 in intimal hyperplasia

Gonzalo Artiach1, Miguel Carracedo1, Joan Clària2, Andres Laguna-Fernandez1, Magnus Bäck1,3

1Department of Medicine, Karolinska Institutet, Stockholm, Sweden, 2Department of Biochemistry and Molecular Genetics, Hospital Clínic-IDIBAPS and Department of Biomedical Sciences, University of Barcelona, Barcelona, Spain, 3Theme Heart and Vessels, Division of Valvular and Coronary Disease, Karolinska University Hospital, Stockholm, Sweden

• In vivo, ChemR23 deletion increased intimal hyperplasia in mice after left carotid artery liga-tion by 59±17%.

• In vitro, ChemR23-/- VSMCs proliferated 40±2% less compared with ChemR23+/+. However, ChemR23-/- macrophages were more pro-in-flammatory, increasing VSMC proliferation by 32±10%.

• The opposing effects of ChemR23 on VSMC pro-liferation suggest a protective role of ChemR23 in intimal hyperplasia under pro-inflammatory con-ditions.

Posters – Monday

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IVBM2018

M063

CDC42 deletion elicits cerebral vascular mal-formations via increased MEKK3-dependent KLF4 expression

Marco Castro1, Bàrbara Laviña1, Koji Ando1, Alberto Álvarez-Aznar1, Cord Brakebusch2, Elisabetta Dejana1,3, Christer Betsholtz1,4, Konstantin Gaengel1

1Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, , Sweden, 2Biotech research & innovation center (BRIC), University of Copenhagen, , Denmark, 3IFOM, the FIRC Institute of Molecular Oncology, Milan, Italy, 4AstraZeneca/Karolinska Integrated Cardio Metabolic Centre (ICMC), Karolinska Institutet, Novum, Huddinge, Stockholm, Sweden

• Inducible endothelial-specific Cdc42 knockout elicits capillary-venous malformations in the cer-ebellum reminiscent of CCM.

• CDC42 is critically required for sprouting angio-genesis, EC axial polarity, and proper dispersion of endothelial cells in the vasculature.

• CDC42-depleted EC exhibit increased KLF2/4 expression through the MEKK3-MEK5-ERK5 path-way, and genetic inactivation of Klf4 hampers the formation of vascular lesions in Cdc42 knockout mice.

M064

Neutrophil extracellular traps accumulate in peripheral vasculature and compromise organ function in mice with cancer

Jessica Cedervall1, Anca Dragomir2, Melanie Herre1, Falk Saupe1, Yanyu Zhang1, Johan Ärnlöv3,4, Erik Larsson2, Anna Dimberg2, Anders Larsson5, Anna-Karin Olsson1

1Department of Medical Biochemistry and MIcrobiology, Uppsala University, Uppsala, Sweden, 2Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 3Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden, 4School of Health and Social Studies, Dalarna University, Falun, Sweden, 5Department of Medical Sciences, Uppsala University, Uppsala, Sweden

• Mice with cancer display impaired function of organs such as kidney and heart.

• Tumor-induced intravascular NETs cause vascu-lar hypoperfusion and inflammation in distant organs.

• Therapeutic targeting of NETs with DNase I or a PAD4 inhibitor suppress inflammation and restore organ function in tumor-bearing mice.

M065

Overexpression of tissue inhibitor of matrix metalloproteinase-3 in human abdominal aor-tic aneurysmal tissues

Yin Tung Crystal Chan1, Wing Keung Stephen Cheng1

1Division of Vascular Surgery, Department of Surgery, The University of Hong Kong, Hong Kong, China

• A significantly overexpressed TIMP3 was observed in human AAA tissues, suggesting TIMP3 overexpression may be associated with aneurysm formation.

• TIMP3 overexpression was observed in tunica media, where VSMCs are localized, of human AAA tissues.

• TIMP3 up-regulation might have an effect of inducing apoptosis of VSMCs in promoting AAA.

M066

Overexpression of reversion-inducing cyste-ine-rich protein with kazal motifs in patients with abdominal aortic aneurysm



• A significant overexpression of RECK in AAA tis-sues from humans, suggesting RECK overexpres-sion may be associated with aneurysm formation.

• RECK up-regulation may represent a physiological attempt to counteract the pathologic increase of MMPs in AAA.

• No significant correlation between RECK protein expression and size of AAA.

M067

Up-regulation of dab2 interacting protein in abdominal aortic aneurysm patients is inde-pendent of rs7025486 polymorphism



• The protein expression of DAB2IP in AAA was sig-nificantly higher than that in control aortic tissues from humans.

• No significant difference in the relative DAB2IP protein expression was observed among the GG, GA, and AA genotypes.

• The novel findings suggested an up-regulation of DAB2IP, independent of the rs7025486 polymor-phism, is associated with AAA.

Posters – Monday

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IVBM2018

M068

Role of microRNA-1260 in vascular smooth muscle cells from human abdominal aortic tissues

Yin Tung Crystal Chan1, Lai Yee Bernice Cheuk1, Wing Keung Stephen Cheng1


• MiR-1260, which was previously found down-reg-ulated in AAA VSMCs, negatively regulates expres-sions of COL1A1 and MCP-1 in human VSMCs.

• Neither expressions of MMP-2, MMP-9, TIMP-1, TIMP-2 nor apoptosis is regulated by miR-1260 in human VSMCs.

• MiR-1260 suppression in VSMCs may up-regulate COL1A1 and MCP-1, possibly promoting compen-satory collagen synthesis and inflammation for AAA formation.

M069

Astrocytic Junctional Adhesion Molecule-A Promotes Central Nervous System Inflamma-tory Lesion Pathogenesis

Candice Chapouly1,2,3,4, Alexandra Gordon2,3,4, Anthony Therattil2,3,4, Pr Gareth John2,3,4, Sam Horng2,3,4

1Umr Inserm U1034, Pessac, France, 2Friedman Brain Institute, New York City, United States, 3Corinne Goldsmith Dickinson Center for Multiple Sclerosis, New York City, United States, 4Neurology, Icahn School of Medicine at Mount Sinai, New York City, United States

• The Blood Brain Barrier (BBB) and Glia limitans (GL) represent a dynamic structure called the gliovascular unit limiting access to the paren-chyma.

• During inflammation, after the BBB opens, the Glia Limitans reacts by producing Claudins and Junctionnal Adhesion molecule A.

• Unlike Claudins which are protective, astrocytic expression of JAM-A promotes leukocyte migra-tion, tissue damage and clinical disability during CNS inflammation

M070

Siglec-E deficiency exacerbates atherosclero-sis in ApoE-deficient mice

Ming-Tsai Chiang1, Dong-Lin Tsai1, Yaw-Wen Hsu1, Paul R. Crocker2, Lee-Young Chau1

1Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, 2Division of Cell Signaling and Immunology, School of Life Sciences, University of Dundee, Dundee, United Kingdom

• The glycan ligand for Siglec-E, a sialic acid-binding immunoglobulin-like receptor expressed on mac-rophages, is detected in atherosclerotic lesions of ApoE-KO mice.

• Siglec-E deficiency accelerates atherosclerosis in ApoE-KO mice without significantly affecting lipid profile.

• Siglec-E deficiency augments oxidized LDL-in-duced foam cell formation in vitro.

M071

Smooth muscle cell reprogramming in aortic aneurysms

Pei-Yu Chen1, Lingfeng Qin1, Guangxin Li1, Zheng Wang1, Sonia Bergaya2, Zehua Chen3, Pengwei Yang3, Nickolas Cilfone3, Sharvari Gujja3, Alexander Caulk1, Sae-Il Murtada1, Xinbo Zhang1, Zhen Zhuang1, Deepak Rao4, Guilin Wang1, Zuzana Tobiasova1, Ruth Montgomery1, Lele Sun5, Hongye Sun5, Edward Fisher2, Jeffrey Gulcher3, Carlos Fernandez-Hernando1, Jay Humphrey1, George Tellides1, Thomas Chittenden3, Michael Simons1

1Yale University, New Haven, United States, 2New York University, New York, United States, 3WuXi NextCODE, Cambridge, United States, 4Harvard Medical School, Boston, United States, 5WuXi NextCODE, Shanghai, China

• Induction of SMC-specific TGFβR2 deletion in adult Apoe-/- mice on a high cholesterol diet led to 100% of animals developing aorta aneurysms.

• A combination of a smooth muscle-specific TGFβR2 knockout and hypercholesterolemia induces aortic SMCs into osteoblasts, chondro-cytes, adipocytes and macrophages.

• scRNA-seq, ChIP-seq, bulk RNA-seq, IMC, CyTOF techniques were used to evaluate fate mapped smooth muscle cells.

Posters – Monday

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IVBM2018

M072

Identification of deubiquitinase USP8 as a novel functional regulator for PDGF-C/PDG-FRα signaling pathway

Rongyuan Chen1, Xiangrong Ren1, Chunsik Lee1, Xuri Li1

1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China

• PDGF-C stimulation resulted in USP8 phosphory-lation in HUVSMC

• USP8 interact with and de-ubiquitinate PDGFRa • Increase expression of USP8 in CNV suggest its

involvement in pathological angiogenesis

M073

Deletion of Rap1 promotes macrophage infil-tration and foam cell formation during athero-sclerosis

Xinyi Chen1,2, Aimin Xu1,2,3, Eva Hoi Ching Tang1,2

1Department of Pharmacology and Pharmacy, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong, China, 2The State Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong, China, 3Department of Medicine, Li Ka Shing Faculty of Medicine, The University of Hong Kong, ,

• Deletion of Rap1 enhances cholesterol uptake in macrophages and its transformation into foam cells through modulation of thiol redox potential.

• eletion of Rap1 increases the migration abil-ity of macrophages by enhancing chemotactic responses towards chemoattractants through modulation of thiol redox potential.

• Deletion of Rap1 promotes atherogenesis by enhancing macrophage recruitment and foam cell formation via modulation of thiol redox stress.

M074

Molecular Regulation of VEGF Signaling by Opposing Endocytic Adaptors

Hong Chen1

1Harvard Medical School, Boston, United States, 2Boston Children’s Hospital, Boston, United States

• Opposing endocytic adaptors epsins and Dab2 interact with VEGFR2 via a mutually exclusive mechanism.

• While Dab2 enhances VEGF signaling, epsins downregulate VEGF signaling.

• Mice lacking endothelial epsins and Dab2 (EC-iTKO) rescue heightened angiogenesis caused by epsin depletion, or attenuated angiogenesis produced by Dab2 loss.

M075

G12/G13-mediated signalling in smooth mus-cle cells is required for vascular myogenic tone regulation

Ramesh Chennupati1, Angela Wirth1, Julie Favre3, Frank Schweda2, Nina Wettschureck1, Daniel Henrion3, Stefan Offermanns1

1Max Planck Institute for heart and lung research, Ludwigstraße 43, Bad Nauheim, Germany, 2Department of Physiology, University of Regensburg, Regensburg, Germany, 3MITOVASC Institute - UMR CNRS 6015 INSERM U1083, University of Angers , Angers, France

• Smooth muscle specific loss of Gα12/Gα13 or its downstream Rho-GEF effector LARG abrogates myogenic tone.

• Lack of Gαq/Gα11 in smooth muscle has no effect on myogenic tone.

• Abrogation of G12/G13-mediated signaling in smooth muscle cells results in hyperperfusion of various organs.

M076

Functional Genetics of Non-Coding Risk Vari-ant in Vascular Dysfunction

Kanxing Wu1, Florence Chioh1, Matias Ilmari Autio3,4, Nicole Pek2, Balakrishnan Chakparani Narmada4, Hwee Hui Lau2, Adrian Teo2, Roger Foo3,4, Mark Chan3, Chew Kiat Heng3, Christine Cheung1,2

1Lee Kong Chian School Of Medicine, Nanyang Technological University, , Singapore, 2Institute of Molecular and Cell Biology, Singapore, 3National University of Singapore, , Singapore, 4Genome Institute of Singapore, , Singapore

• Induced pluripotent stem cells (iPSCs) were gen-erated from coronary artery disease patients car-rying genetic risk variants identified from genome wide association studies.,

• A non-coding risk variant was found to be a dis-tal regulator of atherosclerosis-related genes through long range chromatin interactions.,

• Endothelial cells derived from genetically edited isogenic iPSCs exhibit pathological phenotypes differentially (risk versus non-risk genotypes).

Posters – Monday

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IVBM2018

M077

Role of LYVE-1+ macrophages in Abdominal Aortic Aneurysm

Samantha Chew1, Hwee Ying Lim1, Veronique Angeli1

1National University Of Singapore, Singapore, Singapore

• Loss of LYVE-1+ macrophages in classic ANGII induced AAA apoE−/− mouse model, especially during the early development of AAA.

• Depletion of LYVE-1+ macrophages in AAA-re-sistant wildtype presented key features of AAA including infiltrating macrophages, vascular remodeling and vSMCs apoptosis.

• The plausible role of LYVE-1+ macrophages is maintaining the vasculature via modulating vSMCs survival.

M078

Myocardial canonical Wnt signaling during cardiac development in zebrafish.

Ayano Chiba1, Naoki Mochizuki1

1National Cerebral and Cardiovascular Center Research Institute, Suita, Japan

• We developed a myocardium-specific canonical Wnt signaling reporter fish line.

• The canonical Wnt signaling was activated in the atrioventricular canal.

• Wnt signaling-activated cardiomyocytes might regulate myocardial-endocardial (endothelial) interaction-dependent morphogenesis indepen-dent of known Bmp-Tbx2 axis.

M079

Bitter taste receptors regulate microvascular permeability – a novel role for endothelial bit-ter taste sensing

Ana Couto1, Havovi Chichger1

1Anglia Ruskin University, Cambridge, United Kingdom

• Bitter taste receptors T2R38, T2R14 and T2R10 are highly expressed (mRNA and protein) in the microvasculature

• Agonists for T2R38 and T2R10 attenuate VEGF-in-duced microvascular permeability,

• An agonist for T2R14 worsens permeability in the microvasculature, however molecular inhibition of this bitter taste receptor is barrier-protective

M080

A three-dimensional in vitro model of lymph-angiogenesis in fluidic device

Youngkyu Cho1, Kyuhwan Na2, Ji Hun Yang2, Yesl Jun2, Seok Chung1,2

1Department of IT convergence, Korea University, Seongbok Gu, South Korea, 2School of Mechanical engineering, Korea University, Seongbok Gu, South Korea

• lymphangiogenesis, • 3D cell culture, • microfluidics

M081

The role of Ccm2l in Cerebral Cavernous Mal-formations in neonatal

Jaesung Peter Choi1,2, Xiangjian Zheng1,2

1Lab of Cardiovascular Signaling, Centenary Institute, Sydney, Australia, 2The University of Sydney, Sydney, Australia

• A FDA approved compound is capable of blocking CCM initiation and progression through inhibition of MEKK3 signalling.

• The compound can prevent both the formation of new and the growth of emerged CCM lesions.

• At ultracellular level, this compound can nor-malise the flattening and disorganisation of endo-thelium caused by CCM deficiency.

M082

Potential role of PCSK1 in cholesterol metab-olism

Seungbum Choi1

1Gachon Cardiovascular Research Institute, Incheon, South Korea

• Proprotein Convertases• Cholesterol metabolism• Apolipoprotein A1

Posters – Monday

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IVBM2018

M083

Modeling Hypoxia-Induced Acute Myocardial Infarction in Human Embryonic Stem Cell-De-rived Mature Cardiomyocytes

Seung-Cheol Choi1, Ji-Hyun Choi1, Ha-Rim Seo1, Long-Hui Cui1, Jong-Ho Kim1, Chi-Yeon Park1, Hyung Joon Joo1, Soon Jun Hong1, Do-Sun Lim1

1Department of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul, South Korea

M084

Effect of angiopoietin receptor Tie2 insuffi-ciency on blood vascular and lymphatic ves-sel formation in development

Man Chu1, Taotao Li1, Xudong Cao1, Xiujuan Li1, Yulong He1

1Cyrus Tang Hematology Center,Soochow University, Suzhou, China

• TIE2 is essential for the formation and mainte-nance of veins.

M085

The role of polyunsaturated fatty acid - derived epoxides and diols in angiogenesis and lymphangiogenesis

Giorgia Ciliberti1, Rushendhiran Kesavan1, Sarah Dziumbla1

1Institute For Vascular Signaling, Goethe University Frankfurt, Frankfurt am Main, Germany, 2Institute of Biochemistry I, Goethe-University., Frankfurt am Main , Germany

• Cytochrome P450 derived epoxides and diols.• Vasculogenesis and endothelial specification.• Stem cells differentiation.

M086

Tip Cell Proliferation in Angiogenic Sprouting

Paul Coleman1, Ben Roediger1, Yang Zhao1, Ka Ka Ting1, Angelina Lay1, Wolfgang Weninger1, Mathew Vadas1, Jennifer Gamble1

1Centenary Institute, Sydney, Australia

• Tip cell proliferation occurs in developmental and pathological angiogenesis

• Tip cell proliferation is induced by VEGF and FGF stimulation

• Pericyte coverage inhibits tip cell proliferation

M087

Septin2 Regulates Endothelial Matrix Remod-eling and Angiogenesis

Kerrie Collins1, Hojin Kang1, Jennifer Klomp1,2, Andrei Karginov1, Asrar Malik1

1University Of Illinois At Chicago, Chicago, United States, 2University of North Carolina, Chapel Hill, Chapel Hill, United States

• The filamentous GTPase Septin2 is required for Src-mediated podosome formation in endothelial cells.

• The interaction of Septin2 with the plasma mem-brane via its polybasic domain is necessary for podosomal matrix remodeling to occur.

• Septin2-mediated endothelial matrix remodeling is required for physiological angiogenesis.

M089

Elevated circulating microRNA-126 associates with improved metabolic status of obese dia-betic patients undergoing sleeve gastrectomy

Alina Constantin1, Miruna Nemecz1, Gabriela Tanko1, Alexandru Filippi1, Nicoleta Alexandru1, Habil Adriana Georgescu1, Maya Simionescu1

1Institute of Cellular Biology and Pathology ‘Nicolae Simionescu’, Bucharest, Romania

• Plasma microRNA-126 levels increased 1 year after sleeve gastrectomy in obese type 2 diabetes patients.

• Circulating microRNA-126 negatively correlated with plasma glucose, insulin, and triglycerides, 1 year after sleeve gastrectomy in obese type 2 dia-betes patients.

• Elevated circulating microRNA-126 levels asso-ciated with decreased leptin and increased adi-ponectin may reflect the improvement of vascu-lar function after sleeve gastrectomy.

Posters – Monday

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IVBM2018

M090

Dynamic molecular signatures of cerebral blood vessels during blood brain barrier post-natal development

Sara Cunha1, Lei Conze1, Annalena Wille1, Veronica Sundell1, Elisabetta Dejana1,2,3

1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 2IFOM, FIRC Institute of Molecular Oncology, Milan, Italy, 3Department of Oncology and Hemato-Oncology, University of Milan, Milan, Italy

• Transcriptome profiles of mouse brain ECs during BBB development.

• Comparative analysis between cerebellum and cerebrum.

• Dynamic changes of signaling pathway during BBB development.

M091

Macrophage-specific RIP1 deletion reduces necrotic core formation in atherosclerotic plaques of ApoE knockout mice

Isabelle Coornaert1, Guilia Marcassoli1, Guido De Meyer1, Wim Martinet1

1Laboratory of Physiopharmacology, Department of Pharmaceutical Sciences, University of Antwerp, Antwerp, Belgium

• Macrophage-specific RIP1 gene deletion does not affect the plasma cholesterol level in ApoE-/- mice on western diet.

• Macrophage-specific RIP1 gene deletion reduces significantly plaque size and necrotic core area in ApoE-/- mice on western diet.

• Macrophage-specific RIP1 gene deletion in ApoE-/- mice results into atherosclerotic plaques with a decreased macrophage content.

M092

‘Vessel reassembly’ in the absence of endo-thelial apoptosis as a mechanism for revascu-larising ischemic retinas.

Zoe Grant1,2, Lachlan Whitehead1,2, Vickie Wong3, Zheng He3, Bang V. Bui3, A/Prof R. Andrew Symons3,4,5, Leigh Coultas1,2

1Walter and Eliza Hall Institute of Medical Research, Parkville, Australia, 2University of Melbourne, Department of Medical Biology, Parkville, Australia, 3Department of Optometry and Vision Sciences, University of Melbourne, Parkville, Australia, 4Department of Ophthalmology, Royal Melbourne Hospital, Parkville, Australia, 5Department of Surgery, University of Melbourne, Parkville, Australia

• Blocking apoptosis in the oxygen-induced reti-nopathy model leads to incomplete vessel regres-sion and persistence of non-perfused endothelial cell clusters.

• Endothelial clusters rapidly reassemble back into a functional vascular network upon onset of reti-nal hypoxia.

• ‘Vessel reassembly’ following apoptosis blockade minimizes the duration of retinal hypoxia and prevents neovascular tuft formation.

M093

Functional identification of the genetic deter-minants and markers of vascular regeneration.

Baptiste Coxam1, Holger Gerhardt1

1Max Delbrück Centrum (mdc), Berlin, Germany

• Our research plan aims to unravel the nature, origin and function of single-cell heterogeneity throughout the vascular endothelium during cau-dal fin regeneration.

• In a translational line-of-sight, we expect that identifying candidate genes contributing to innate or adaptive response to vascular injury will provide us with testable targets for regenerative cardiovascular medicine.

Posters – Monday

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IVBM2018

M094

The Role of Meis Transcription Factors in the Epicardium

Ester Cruz-Crespillo1, Noelia Muñoz-Martín1, Vanessa Cadenas1, Miguel Torres1

1Cnic, Madrid, Spain

• Meis transcription factors are expressed in the epicardium

• The lineage of Meis1-expressing cells contributes to different cardiac cell types, including epicardial and endothelial cells.

• Epicardial-specific Meis1 and Meis2 deletion does not provoke functional alterations but coro-nary vasculature is altered.

M095

ScRNAseq of brain CCM-deficient endothe-lium reveals cell populations with endothelial and mesenchymal characteristics

Sara I Cunha1, Lei Liu Conze1, Johan Brännström1, Annalena Wille1, Veronica Sundell1, Peetra Magnusson1, Elisabetta Dejana1,2

1Uppsala University; Department of Immunology. Genetics and Pathology, Uppsala, Sweden, 2FIRC Institute of Molecular Oncology, Milan, Italy

• Endothelial cell heterogeneity in CCM deficient vasculature

• Single cell RNA sequencing to dissect endothelial cell heterogeneity

• Cell subpopulations displaying novel subsets of mesenchymal markers

• Targeted therapy aiming the novel markers

M096

The dorsal skin fold chamber as a model for intravital confocal microscopy

Silke Currie1, Kerstin Schäfer1, Stefan Volkery1, Bernhard Nieswandt2, Stefan Butz1, Dietmar Vestweber1

1Max-Planck Institute for Molecular Biomedicine, Münster, Germany, 2Rudolf-Virchow Zentrum Universität Würzburg, Würzburg, Germany

• We established the dosal skin fold chamber as a confocal intravital imaging model to study throm-bocytopenia in vivo.

• In the absence of platelets, our results indicate that neutrophil extravasation destabilizes con-tacts, leading to temporary loss of vascular integ-rity.

• Our data support the idea that single platelets bind to challenged endothelial contacts, follow-ing neutrophil extravasation.

M097

Diverse functional vasomotor responses between aorta and inter-lobar renal arteries in LdlrKO mice

Katrine Dahl Bjørnholm1,2, Gry Freja Skovsted1, Pernille Tveden-Nyborg1, Günaj Rakipovski2, Gro Klitgaard Povlsen2, Jens Lykkesfeldt1

1Univeristy Of Copenhagen, Department of experimental animal models , Frederiksberg, Denmark, 2Novo Nordisk, Global Reseach, Måløv, Denmark

• Functional vasomotor responses of inter-lobar renal arteries were characterized and compared to thoracic aorta in the LdlrKO

• The aorta, but not the inter-lobar renal artery, show decrease contractile and dilatory responses compared to age matched controls

• These effects were amplified to some extend by a westernized diet

M098

Development and function of adult specific lymphatics in the zebrafish fins

Rudra Das1, Karina Yaniv1


• We investigate context-dependent post-embry-onic lymphangiogenesis in newly developed tis-sues and regeneration, utilizing endothelial spe-cific multicolour lineage tracing tool.

• Our study uncovers important features of post-embryonic lymphangiogenesis, indicating a previously unknown role in promoting tissue morphogenesis.

• In regenerating fins, the lymphatic vasculature is first to regenerate and influences immune cell trafficking, indicating a pro-regenerative role.

Posters – Monday

– 50 –

IVBM2018

M099

The complex role of lactate dehydrogenases in glioblastoma development and vasculariza-tion

Thomas Daubon1,2, Heidi Espedal2, Tiffanie Chouleur5, Nina Obad2, Céline Leon1, Pr Hrvoje Miletic2,3,4, Rolf Bjerkvig2,4,5, Andreas Bikfalvi1

1Inserm U1029 - Bordeaux University, BORDEAUX, France, 2NorLux Neuro-Oncology, Department of Biomedicine, University of Bergen, BERGEN, NORWAY, 3Department of Pathology, Haukeland University Hospital , BERGEN, NORWAY, 43KG Jebsen Brain Tumour Research Center, University of Bergen, BERGEN, NORWAY, 5Nor-Lux Neuro Oncology Laboratory, LIH, LUXEMBOURG , LUXEMBOURG

• Lactate dehydrogenase B in tumor angiogenesis• Complex roles of LDHA and LDHB in glioblastoma

development • Double LDHA/LDHB knock-out tumors with

impaired development

M100

Molecular regulation of acute Tie2 suppres-sion in sepsis

Idowu Temitayo1, Claudia Schrimpf1, Jennifer Retzlaff1, Matjis van Meurs3, Chandra Ghosh2, Samir Parikh2, Sascha David1

1Medical School Hannover, Hannover, Germany, 2Beth Israel Deaconess Medical Center & Harvard Medical School, Boston, USA, 3University Medical Center Groningen, Groningen , The Netherlands

• Endothelial Tie2 expression is acutely downregu-lated in models of systemic inflammation by two different mechanisms

• On the protein level, the matrix metalloprote-ase MMP14 is both necessary and sufficient for N-terminal Tie2 shedding

• On the transcriptional level, Tie2 mRNA is nega-tively regulated upon reduced exposure to flow (a hallmark of shock) via the transcription factor GATA3.

M101

Protein determinants and contractile conse-quences of the media-to-lumen ratio in arter-ies of cardiovascular disease patients

Maria Bloksgaard1, Thomas Leurgans1, Hans Kristian Beck2, Ahkmadjon Irmurhadmekov2, Jo G. R. De Mey1,2

1University of Southern Denmark, Odense, Denmark, 2Odense Unversity Hospital, Odense, Denmark

• Is the M:L of resistance arteries from patients positively associated with contractile function and presence of contractile smooth muscle mark-ers?

• In resistance arteries from 128 patients with residual cardiovascular disease, this is not the case.

• Resistance artery structure and contractile func-tion seem distinct phenotypes differentially related to the basement membrane, sympathetic nerves and a cytokine.

M102

Defective autophagy in vascular smooth mus-cle cells alters vascular reactivity in young C57Bl6 mice

Dorien De Munck1, Paul Fransen1, Sofie De Moudt1, Lynn Roth1, Guido De Meyer1, Wim Martinet1

1Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium

• Mice with an autophagy deficiency in VSMC show increased voltage-gated calcium channels sensi-tivity in the aorta and femoral artery.

• SR-mediated contractions were only affected in the femoral artery segments of autophagy defi-cient mice.

• Aortic segments of autophagy deficient mice show increased basal NO, whereas femoral artery segments were more sensitive to exogenous NO

Posters – Monday

– 51 –

IVBM2018

M103

Aortic microcalcification is caused by elastin peptide-induced ERK1/2 signaling in Marfan smooth muscle cells.

Shaynah Wanga1, Stijntje Hibender1, Yanto Ridwan2, Barbara Mulder3, Carlie de Vries1, Jeroen Essers2, Vivian De Waard1

1Dept. Medical Biochemistry, Academic Medical Center, Amsterdam, Netherlands, 2Dept. of Molecular Genetics, Erasmus MC, Rotterdam, Netherlands, 3Dept. Cardiology, Academic Medical Center, Amsterdam, Netherlands

• Elastin degradation in Marfan aorta associates with local microcalcification.

• Elastin fragments promote an osteogenic phe-notype in aortic smooth muscle cells via ERK1/2 signaling.

• Aortic microcalcification imaging may be of prog-nostic value to detect disease progression in Mar-fan Syndrome.

M104

Toll-like receptor 3 prevents vein graft dis-ease via type-I interferon induced reduction of inflammatory responses

Margreet De Vries1, Karin Simons1, Erna Peters1, Wouter Jukema2, Paul Quax1

1Department of Surgery, Leiden University Medical Center, Leiden, Netherlands, 2Department of Cardiology, Leiden University Medical Center, Leiden, Netherlands

• TLR3 is preventive in vein graft disease via Inter-feron Regulatory Factors 3 and 7.

• IRF3 and IRF7 induce type-I IFN and type-1 IFN inducable genes upon TLR3 ligand stimulation.

• Induction of pro-inflammatory cytokines in vein graft disease is IRF3 dependent but not IRF7 dependent.

M105

Effect of flavonoid metabolites and related phenolic acids on leukocyte trans endothelial migration

Nursabah Atli1,2, Alexandre Motta2, Maria O’Connell1, Andrew Beekman1, Colin Kay3, Mark Searcey1, Paul Oranje2, Felicia Kartawidjajaputra2, Olivia Mühlbauer2, Saurabh Prabhu1, Richard Draijer2

1School of Pharmacy, University of East Anglia, NR4 7TJ, Norwich, United Kingdom, 2Unilever Research and Development Vlaardingen B.V., Olivier van Noortlaan 120, 3133 AT, Vlaardingen, Netherlands, 3Department of Food, Bioprocessing and Nutrition Sciences, Plants for Human Health Institute, 600 Laureate Way, Kannapolis, NC 28081, Kannapolis, USA

• Flavonoid intake is associated with a reduced risk of CVD and these compounds are commonly metabolised to phenolic acids,

• We investigated the effects and structure activ-ity relationship of 20 phenolic acids on fMLP-in-duced trans-endothelial migration of leukocytes,

• Four phenolic acids significantly reduced mono-cyte migration, with three of these containing a single halogen substitution.

M106

Functional role of midkine in arteriogenesis

Elisabeth Deindl1,2, Thomas Lautz1, Manuel Lasch1,2, Julia Borgolte1, Judith-Irina Pagel1, Kerstin Troidl3, Amelia Caballero-Martinez1, Eike Kleinert1, Barbara Walzog1,2

1Walter-Brendel-Centre of exp. Medicine, Munich, Germany, 2Biomedical Center, Munich, Germany, 3MPI for Heart and Lung Research, Bad Nauheim, Germany

• Midkine is decisive for endothelial cell prolifera-tion in arteriogenesis,

• Leukocyte domiciled midkine controls the bio-availability of plasma VEGF-A mediating endothe-lial Nos1 and Nos3 expression,

• eNOS/nNOS, relevant for endothelial cell prolifer-ation in arteriogenesis, can substitute each other

Posters – Monday

– 52 –

IVBM2018

M107

Hematopoietic PHD3 deficiency increases atherosclerotic plaque size in mice

Jasper Demandt1, Elke Marsch1, Han Jin1, Kim van Kuijk1, Thomas Theelen1, Peter Carmeliet2,3, Judith Sluimer1

1Department of Pathology, CARIM, MUMC+, Maastricht, Netherlands, 2Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven, Belgium, 3Laboratory of Angiogenesis and Neurovascular Link, Department of Oncology, KU Leuven, Leuven, Belgium

• PHD3 expression is upregulated in human unsta-ble atherosclerotic plaques

• PHD3 expression correlates with pro-atherogenic plaque characteristics in human plaques

• Murine hematopoietic PHD3 deficiency enhances plaque size and necrotic content likely through enhanced macrophage apoptosis

M108

Genetic deletion of BMP9 in 129/Ola mice causes liver sinusoidal endothelial cell capil-larization and fibrosis

Agnes Desroches-castan1, Emmanuelle Tillet1, Marie Ouarné1, Christine Mallet1, Sabine Bailly1, Jean-Jacques Feige1

1University Grenoble-Alpes, INSERM, CEA, Biosciences and Biotechnology Institute of Grenoble, Biology of Cancer and Infection Lab., , Grenoble, France

• Bmp9-KO mice die prematurely in the 129/Ola genetic background but not in the C57BL/6 back-ground.

• 129/Ola Bmp9-KO mice present hepatic fibrotic alterations.

• Genetic loss of BMP9 leads to Liver Sinusoidal Endothelial Cells capillarization in 129/Ola back-ground.

M109

Cell lineage studies of cerebral cavernous malformations(CCMs): evidence of a single mutation initiating individual CCMs

Matthew Detter1,2, Amy Peiper1, Heidy Pardo1, Carol Gallione1, Erin Griffin1, Douglas Marchuk1

1Department of Molecular Genetics and Microbiology, Duke University School of Medicine, Durham, United States, 2Medical Scientist Training Program, Duke University School of Medicine, Durham, United States

• We simultaneously induce CCM allele deletion and Brainbow recombination to generate fluo-rescently-tagged mutant endothelial cells in a mouse model

• Confocal microscopy and 3D reconstruction demonstrates that CCMs are composed of mutant cells with the same fluorescent protein color

• Single mutation event, as evidenced by a single color within the induced CCMs, is sufficient to drive malformation pathogenesis

M110

Improved survival and immunostimula-tory reprogramming in a glioblastoma model by combining anti-angiogenic and immune-checkpoint therapy

Mariangela Di Tacchio1, Jadranka Macas1, Jakob Weissenberger1, Kathleen Sommer1, Kavi Devraj1,2, Stefan Guenther5, Karl H. Plate1,3,4, Yvonne Reiss1,3,4

1Institute of Neurology (Edinger Institute), Frankfurt am Main, Germany, 2Pharma Zentrum, Goethe University Hospital, Frankfurt am Main, Germany, 3German Cancer Consortium (DKTK), Partner Site Frankfurt / Mainz, Germany, 4German Cancer Research Center (DKFZ), Heidelberg, Germany, 5Max Planck Institute for Heart and Lung , Bad Nauheim, Germany

• Standard therapy of glioblastoma multiforme evokes only modest advances in patient survival, therefore new treatment options are urgently needed.

• In a preclinical glioblastoma model, PD-1 inhi-bition led to extended survival post anti-VEGF/Ang-2 therapy by creating an immunostimulatory microenvironment.

• Moreover, anti-angiogenic therapy led to vascu-lar normalization at the morphological and gene expression level.

Posters – Monday

– 53 –

IVBM2018

M111

Primary cilia affect the endothelial response to aneurysmal wall shear stress

Mannekomba Diagbouga1, Sandrine Morel1, Sylvain Lemeille1, Beerend Hierck3, Philippe Bijlenga2, Brenda Kwak1

1Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland, 2Department of Clinical Neurosciences, Geneva University Hospitals, , Switzerland, 3Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands

• In response to aneurysmal wall shear stress (WSS), endothelial cells (EC) lacking primary cilia have 5-fold more genes and distinct pathways regulated compared to wild-type ECs.

• RNA-Seq showed a differential regulation of cell adhesion/tight junction pathways in response to aneurysmal WSS in ECs with and without primary cilia.

• Cilium-deficient ECs present enhanced permea-bility compared to wild-type ECs.

M112

Thioredoxin interacting protein endothelial reduced expression protects from metabolic stress-induced impaired angiogenesis in adult mice

Alison Domingues1,2, Jérémy Sadoine3, Blandine Dizier1,2, David Smadja1,2,4, Catherine Chaussain3, Catherine Boisson-Vidal1,2, Valérie Nivet-Antoine1,2,5

1INSERM, UMRS1140 - IThEM, Paris, France, 2Faculty of Pharmacy, Paris Descartes University, Sorbonne Paris Cité, Paris, France, 3Laboratoire EA2496 et Plateforme d’Imagerie du Vivant (PIV), Paris Descartes University, Sorbonne Paris Cité, Montrouge, France, 4Department of Hematology, Georges Pompidou European Hospital, Assistance Publique-Hôpitaux de Paris (AP-HP), Paris, France, 5Clinical Biochemistry, Necker Hospital, AP-HP, Paris , France

• Reducing endothelial TXNIP prevents from vessel area and number of sprouts HP-LC-induced-de-crease in the aortic ring assay

• Reducing endothelial TXNIP protects from a HP-LC-induced-decrease of blood flow (laser dop-pler), decrease of thigh vascular density, total segment number and smaller arteries number (microCT) in the hindlimb ischemia model

• Protection against inflammation cells and adipo-cytes infiltration and myofibers necrosis

M113

Differential but complementary HIF1α and HIF2α transcriptional regulation in endothelial cells

Nicholas Downes1, Nihay Laham-Karam1, Minna Kaikkonen1, Seppo Ylä-Herttuala1,2

1A.I. Virtanen Institute for Molecular Sciences, UEF, Kuopio, Finland, 2Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• In endothelial cells, HIF1α and HIF2α differen-tially regulate the expression of 701 and 1454 genes, respectively

• HIF1α primarily regulated metabolic reprogram-ming processes, whereas HIF2α predominantly regulated angiogenic extracellular signalling, guidance cues and extracellular matrix remodel-ling factors

• HIF2α uniquely regulated a surprisingly diverse array of transcription factors which may contrib-ute to its context dependent roles in hypoxia

M114

VEGFR2 and VEGF-C Suppress the Epithelial–Mesenchymal Transition via YAP in RPE Cells

Yuxiang Du1, Qishan Chen2, Lijuan Huang2, Shasha Wang2, Xiangke Yin1, Xuri Li2, Rong Ju2

1Sun Yat-sen University, guangdong, guangzhou, China, 2State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, guangdong, guangzhou, China

• We show that knockdown of VEGFR2 results in epithelial-mesenchymal transition (EMT) and overexpression of

• VEGFR2 suppresses TGF β-mediated EMT in RPE cells.

• We further reveal that loss of VEGF-C rather than VEGF-A induces EMT.

• The VEGFR2 ablation-induced EMT in RPE cells is mediated by activation of YAP, an effector of the Hippo pathway.

Posters – Monday

– 54 –

IVBM2018

M115

NCK-dependent pericyte migration promotes pathological neovascularization in ischemic retinopathy

Alexandre Dubrac1, Künzel S.E.1, Künzel S.H.1, Li Jinyu1, Rachana Radhamani Chandran1, Kathleen Martin1, Daniel M. Greif1, Adams R.H.2, Anne Eichmann1,3,4

1Yale Cardiovascular Research Center, Department of Internal Medicine, New Haven, United States, 2Max Planck Institute for Molecular Biomedicine, Department of Tissue Morphogenesis and University of Münster, Faculty of Medicine, Münster, Germany, 3INSERM U970, Paris Cardiovascular Research Center, Paris, France, 4Department of Cellular and Molecular Physiology, New Haven, United States

• Characterization of retinal pericytes in devel-opment and oxygen-induced retinopathy (OIR) model.

• NCK1 and 2 signaling downstream of PDGFRβ promotes PDGF-B-induced pericyte migration in vivo and in vitro.

• Pericyte specific deletion of Nck1&2 inhibited pathological angiogenesis, while retinal revascu-larization was improved in OIR.

M116

Abrogation of Fzd7 protects against the development of pathological angiogenesis in ischemic retinopathy

Marie Lise Bats1, Camille Seguy1, Claire Peghaire2, Sylvie Jeanningros1, Béatrice Jaspard1, Pr Thierry Couffinhal1, Cécile Duplàa1, Pascale Dufourcq1

1Inserm U1034, University of Bordeaux, Bordeaux, France, 2National Heart & Lung Institute, Vascular Science, Imperial Centre for Translational and Experimental Medicine, Imperial College London, Hammersmith Hospital, London , United Kingdom

M117

Systemic endothelial ERG deletion leads to tissue-specific vascular remodelling

Neil Dufton1, Claire Peghaire1, Viktoria Kalna1, Linda Inuabasi1, Graeme Birdsey1, Anna Randi1

1Imperial College London, London, United Kingdom

• Chronic ERG deficiency resulted in systemic fibro-genic phenotype.

• Lung and liver tissue had substantial disruption of the vascular and tissue architecture, together with increased leukocyte infiltration, haemor-rhage and enhanced SMAD3 activity.

• Vascular remodeling in the kidney occured inde-pendently of pSMAD3

• The endothelial (EC)-specific transcription fac-tor ERG is constitutively expressed in all vascular beds. We recently showed that short-term ERG deletion within the liver causes TGFβ-SMAD3-induced endothelial-to-mesenchymal transition (EndMT) and liver fibrogenesis. This study aimed to determine the systemic effects of chronic ERG deletion on vascular and tissue homeostasis.

M118

A systems-based approach reveals human nestin is an angiogenesis-independent, endo-thelial-enriched, shear-modulated intermedi-ate filament

Philip Dusart1,2, Linn Fagerberg1, Ljubica Persic Matic3, Mete Civelek4, Eike Struck1, Ulf Hedin3, Mathias Uhlén1, David-Alexandre Trégouët5, Thomas Renné6, Jacob Odeberg1,7, Lynn Butler1,2

1Science for Life Laboratory, Kungliga Tekniska Högskolan (KTH), Stockholm, Sweden, 2Clinical Chemistry and Blood Coagulation, Karolinska Institute, Stockholm, Sweden, 3Vascular Surgery, Karolinska Institute, Stockholm, Sweden, 4Department of Biomedical Engineering, University of Virginia, Charlottesville, USA, 5ICAN Institute for Cardiometabolism and Nutrition, Paris, France, 6Institute for Clinical Chemistry and Laboratory Medicine, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany, 7Coagulation Unit, Centre for Hematology, Karolinska University Hospital, Stockholm, Sweden

• Nestin is constitutively expressed throughout the adult human vasculature, independent of angio-genesis, challenging the current dogma that it is a marker of proliferation

• Subcellular distribution of nestin is shear-modu-lated, and reduced expression is associated with proliferation and neovessels in atherosclerotic plaques.

• eQTL analysis reveals an association between car-diovascular disease and reduced aortic EC nestin mRNA expression

Posters – Monday

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IVBM2018

M119

Adventitial interleukin-6 release is critical for neointima formation

Jochen Dutzmann1, Jan-Marcus Daniel1, Laura Korte1, Frederik Kloss1, Mirja Sirisko1, Stefan Offermanns2, Kevin J Croce3, Johann Bauersachs1, Daniel G Sedding1

1Hannover Medical School, Hannover, Germany, 2Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany, 3Harvard Medical School, Boston, USA

• Acute vascular injury is followed by an expansion of cytokine-producing adventitial cells.

• The paracrine function and especially the release of IL-6 is essential for the subsequent induction of the proliferation and migration of local SMCs and thus for neointima formation.

• Advetitial cells do not transdifferentiate into neointimal smooth muscle cells.

• The aim of this study was to analyze the impact of the adventitial layer on vascular remodeling pro-cesses.

M120

The role of CD73 in afferent lymphatics

Dominik Eichin1, Juha Laurila1, Lydia Bellmann3, Patrizia Stoitzner3, Nikolaus Romani3, Sirpa Jalkanen1, Marko Salmi1,2

1Medicity Research Laboratory, University of Turku, Turku, Finland, 2Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland, 3Department of Dermatology, Innsbruck Medical University, Innsbruck, Austria

• CD73 exerts various anti-inflammatory effects.• CD73 is expressed on afferent lymphatics.• Afferent lymphatic CD73 has anti-inflammatory

effects on passing, migratory immune cells.

M121

Venous specific development and fluid homeostasis in the retina

Harri Elamaa1,2, Minna Kihlström1,2, Ilkka Miinalainen2, Marjut Nätynki1,2, Lauri Eklund1,2

1Faculty of Biochemistry and Molecular Medicine, Oulu, Finland, 2Biocenter Oulu, University of Oulu, Oulu, Finland

• We investigated the importance of venous drain-age for fluid clearance in the retina by targeting Ang/Tie signaling pathway.

• Defective venous development resulted in neu-ronal cell swelling and displaced processes of Müller glia.

• Our study identifies new mechanism for venous-specific development, insights for patho-genesis of retinal edema, and complementary roles for angiopoietins to establish the retinal cir-culatory system.

M122

Endothelial-Derived Exosome Biomarkers Suggest Activation of Innate Immunity in Sub-clinical Cerebrovascular Disease

Fanny Elahi1, Marie Altendahl1, Kaitlin Casaletto1, Adam Staffaroni1, Evan Fletcher2, Jason Hinman3, Charles DeCarli2, Edward Goetzl1, Joel Kramer1

1University Of Califoria San Francisco, San Francisco, United States, 2University of California Davis, Davis, United States, 3University of California Los Angeles, Los Angeles, United States

• Endothelia-derived exosomes (EDE) provide a non-invasive means of studying vascular endo-thelial disease in vivo

• EDE biomarkers suggest the development of a cerebral inflammatory milieu in subclinical cere-bral small vessel disease

• EDE proteins can provide biological insight into molecular differences in diseased versus healthy vascular endothelia

Posters – Monday

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IVBM2018

M123

Inducible endothelial cell deletion of pro-lyl-4-hydroxylase-2 results in pulmonary hypertension and fibrosis without arterial remodeling

Harri Elamaa1, Marjut Nätynki1, Zoltan Szabó2, Risto Kerkelä2, Johanna Myllyharju1, Joni Mäki1, Mika Kaakinen1, Lauri Eklund1

1Oulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, Biocenter Oulu, University of Oulu, , Finland, 2Medical Research Center Oulu, Research Unit of Biomedicine, University of Oulu and University Hospital Oulu, , Finland

• Inducible endothelial cell deletion of Phd2 results in pulmonary hypertension and structural remod-eling in pulmonary microvasculature.

M124

Gene therapy with Angiotensin-(1-9) inhibits neointima formation in a murine model of vas-cular injury

Sammy El-Mansi1, Stacy Robertson1, Andrew James Irwin1, Angela Catherine Bradshaw1, Stuart Anthony Nicklin1

1University of Glasgow , Glasgow , United Kingdom

• Exogenous Ang-(1-9) peptide inhibits human saphenous vein smooth muscle cell (HSVSMC) proliferation and migration

• Conditioned media from RAdAng-(1-9) trans-duced HepG2 cells inhibits serum induced HSVSMC proliferation

• Systemic delivery of RAdAng-(1-9) attenuates neointima formation after wire injury in mice

M125

Pericyte-specific deletion of the matricellular protein CCN1 changes the angiogenic out-come in ischemic retinopathy

Brahim Chaqour1, Menna Elaskandry, Sangmi Lee1Suny Downstate Medical Center, Brooklyn, United States

• CCN1 is a vascular matrix protein produced by angiogenic endothelial cells during development and by pericytes under ischemic conditions.

• Deletion of pericyte-derived CCN1 reduces neo-vascular growth in a mouse model of ischemic retinopathy by inhibiting secretion of Wnt5a.

• CCN1-pericyte communication elicits paracrine signals (e.g., Wnt5a) that alter normal endothelial cell behavior under ischemic conditions.

M126

Endothelial AMPK controls insulin-dependent myocardial blood flow and left ventricular function

Erik van Poelgeest1, Beate Fisslthaler2, Melissa Verkaik1, Anna Emanuel3, Ingrid Fleming2, Erik Serne3, Yvo Smulders3, Victor van Hinsbergh1, Etto Eringa1

1Department of Physiology, VU University Medical Centre, Amsterdam, Netherlands, 2Institute for Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany, 3Department of Internal Medicine, VU University Medical Centre, Amsterdam, Netherlands

• Physical activity enhances insulin-induced micro-vascular recruitment in the myocardium of men and mice.

• Insulin-induced microvascular recruitment cor-relates with left ventricular function in healthy human subjects.

• The exercise-activated kinase AMPK in endo-thelium regulates insulin-induced microvascular recruitment and left ventricular function by alter-ing expression of cardiomyocyte proteins associ-ated with contraction, actin cyto-skeleton organi-zation and response to stress

M127

A novel S1P1 agonist reduces endothelial dysfunction in a rat model of type 2 diabetes

Maria Francesca Evaristi1, Catherine Cadrouvele1, Brigitte Molinier2, Marie-Pierre Pruniaux1, Philip Janiak1, Bruno Poirier1, Ashfaq Parkar3

1Sanofi R&D, Cardiovascular & Metabolism Therapeutic Area, Chilly-Mazarin, France, 2Sanofi R&D, TMED Biomarkers & Clinical Bioanalysis, Montpellier, France, 3Sanofi R&D, Cardiovascular & Metabolism Therapeutic Area, Bridgewater, US

• A novel biased S1P1 agonist (Compound SA) improves glomerular endothelial barrier integrity in type 2 diabetic ZDF rats.

• Plasma biomarkers of endothelial dysfunction and inflammation including sICAM-1 and CRP were reduced by Compound SA in ZDF rats.

• Sustained S1P1 activation with Compound SA may be a promising treatment to restore endo-thelial function in T2D-related diseases.

Posters – Monday

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IVBM2018

M128

Apocynin abolishes AngII-induced contraction in renal hypertensive (2K-1C) rat aortas

Bernah Fahning1, Marcella Grando1, Lusiane Bendhack1

1Faculty Of Pharmaceutical Sciences Of Ribeirão Preto- Usp, Ribeirão Preto, Brazil

• Nox plays a key role in AngII-induced contractile response

• Endothelium has an anti-contractile effect in AngII-induced contraction in 2K-1C aortas

• eNOS and COX do not play important role in AngII-induced contraction in 2K-1C rat aortas

M129

Robo4 – a new regulator for naïve B cell egress from Peyer’s patches

M.Sc. Ruth Fair-Mäkelä1, Milas Ugur2, Imtiaz Iftakhar-E-Khuda1, Anu Kukkonen-Macchi1, Oliver Pabst2, Kati Elima1,3, Masayuki Miyasaka1,4, Sirpa Jalkanen1,5

1MediCity Research Laboratory, University Of Turku, Turku, Finland, 2Institute of Molecular Medicine, RWTH University, Aachen, Germany, 3Department of Medical Biochemistry and Genetics, University of Turku, Turku, Finland, 4Immunology Frontier Research Center, Osaka University, Osaka, Japan, 5Department of Medical Microbiology and Immunology, University of Turku, Turku, Finland

• Lymphocytes migrate into lymph nodes via the blood vessels or afferent lymphatics and egress via the efferent lymphatics.

• To characterize the molecular differences between the afferent and efferent lymphatics, we performed a genome-wide microarray study.

• Robo4, an endothelial cell molecule predomi-nantly expressed in the efferent lymphatics, reg-ulates the egress of naïve B cells from the Peyer’s patches.

M130

Reducing VEGF-B signaling ameliorates renal lipotoxicity and protects against diabetic kid-ney disease

Annelie Falkevall1, Annika Mehlem1, Isolde Palombo1, Benjamin Heller Sahlgren1, Lwaki Ebarasi1, Liqun He2, Jimmy Ytterberg3, Hannes Olauson4, Jonas Axelsson1, Birgitta Sundelin5, Jaakko Patrakka6, Pierre Scotney7, Andrew Nash7, Ulf Eriksson1

1Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, stockholm, Sweden, 2Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, Uppsala , Sweden , 3Division of Physiological Chemistry I, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden, 43Division of Renal Medicine, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden, 5Department of Oncology-Pathology, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden , 6KI/AZ Integrated CardioMetabolic Center (ICMC), Department of Laboratory Medicine, Karolinska Institutet , Huddinge, Sweden, 7CSL Limited, Parkville, Victoria, Australia

• Targeting VEGF-B signaling reduces renal lipotox-icity prevents DKD

• The beneficial effect is due to re-sensitizing podo-cytes to insulin signaling

• Renal VEGF-B levels are increased in both experi-mental models and subjects with DKD

M131

Microcirculatory perfusion disturbances and endothelial hyperpermeability following car-diopulmonary bypass persist in the early postoperative period

Nicole Dekker1,2, Anoek van Leeuwen1,2, Peter Hordijk2, Alexander Vonk3, Christa Boer1, Charissa van den Brom1,2

1Department of Anaesthesiology, VU University Medical Center, Amsterdam, Netherlands, 2Department of Physiology, VU University Medical Center, Amsterdam, Netherlands, 3Department of Cardiothoracic Surgery, VU University Medical Center, Amsterdam, Netherlands

• Cardiopulmonary bypass is associated with micro-circulatory perfusion disturbances, increased endothelial permeability and altered angiopoie-tin/Tie2 signalling.

• Microcirculatory perfusion disturbances and endothelial hyperpermeability following CPB per-sist in the first three postoperative days

• Cardiopulmonary bypass-associated impair-ment of microcirculatory perfusion and in vitro endothelial barrier function are associated with increased plasma levels of angiopoietin-2.

Posters – Monday

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IVBM2018

M132

VEGF-C promotes hematopoietic regeneration by regulating perivascular niche

Shentong Fang1,2, Shuo Chen2, Harri Nurmi1,2, Veli-Matti Leppänen1,2, Micheal Jeltsch1,2, Hanna Mikkola3, Kari Alitalo1,2

1Wihuri Research Institute, Finland, 2Translational Cancer Biology Program, University of Helsinki,, Finland, 3Department of Molecular, Cell and Developmental Biology, Eli and Edythe Broad Stem Cell Research Center, University of California, Los Angeles, USA

• In the adult BM, Vegfc mRNA is highly expressed in bone marrow endothelial cells and LepR+ cells.

• During homeostasis, VEGF-C maintains the bone marrow (peri-)vascular niche.

• Niche-derived VEGF-C is crucial for hematopoi-etic recovery after irradiation.

M133

Mechanical regulation of endothelial cell metabolism

Yun Fang1, David Wu1, Ru-Ting Huang1, Robert Hamanaka1, Gokhan Mutlu1

1The University Of Chicago, Chicago, United States

• Hemodynamic forces are major regulators of endothelial cell metabolism.

• Disturbed blood flow associated with atheroscle-rosis induces glycolysis and reduces mitochon-drial respiratory capacity in aortic endothelium while unidirectional flow promotes oxidative phosphorylation.

• Disturbed flow-induced metabolic reprogram-ming requires hypoxia inducible factor-1a (HIF-1a), which is stabilized by NOX4-derived reactive oxygen species (ROS).

M134

Coronary Artery Disease Locus 1p32.2 Har-bors a Flow-Sensitive Endothelial Enhancer that Regulates PLPP3

Prof Yun Fang1, Matthew Krause1, Mete Civelek2, Casey Romanoski3

1The University of Chicago, Chicago , United States, 2The University of Chicago, Chicago , United States, 3The University of Virginia , Charlottesville, United States, 4The University of Arizona, Tucson , United States

• Coronary artery disease (CAD) locus 1p32.2 har-bors a mechano-sensitive endothelial enhancer that regulates PLPP3 expression.

• CAD protective allele at rs17114036 confers an increased enhancer activity that is dynamically regulated by unidirectional flow and KLF2.

• Human haplotypes and related cis-regulatory ele-ments provide a previously unappreciated layer of regulatory control in cellular mechano-sensing mechanisms related to atherosclerosis.

M135

Vascular Network Mapping of Whole Mouse Organs with Knife Edge Scanning Microscopy

Corey Monteith1, Venkata N. P. Vemuri1, Navid Farahani1

13scan, Inc., San Francisco, United States

• 3D mapping of vascular networks has been virtu-ally impossible with thin section histology

• Using Knife Edge Scanning Microscopy, we have developed a multiparametric vascular network analysis

• We compare wild-type and transgenic murine organ-wide vasculature networks via branch point count, branch length, vessel radius, and tor-tuosity

Posters – Monday

– 59 –

IVBM2018

M136

The CCM 1/2 complex orchestrates ROCK1 and ROCK2 complementary functions to maintain endothelial mechanical integrity

Justyna Lisowska1, Claudia Rödel2, Yekaterina Miroshnikova1, Sandra Manet1, Cyril Boyault1, Emmanuelle Planus1, Olivier Destaing1, Gwénola Boulday4, Elisabeth Tournier-Lasserve4, Martial Balland3, Salim Abdelilah-Seyfried2,5, Corinne Albiges-Rizo1, Eva Faurobert1

1CNRS UMR5309 Inserm U1209, Grenoble, France, 2Institute of Biochemistry and Biology, Potsdam University, Potsdam, Germany, 3CNRS UMR 5588 LIPhy, Grenoble, France, 4INSERM, UMR-S1161, Paris, France, 5Institute of Molecular Biology, Hannover Medical School, Hannover, Germany

• ROCK1 and ROCK2 have complementary roles on the endothelial mechanical homeostasis.

• The Cerebral Cavernous Malformation (CCM) 1/2 complex functions as a scaffold promoting the interaction of ROCK2 with VE-cadherin and limit-ing ROCK1 kinase activity.

• Silencing of ROCK1, not ROCK2, restores the con-tractile homeostasis of CCM1/2-depleted endo-thelial monolayers as well as cardiovascular mal-formations in ccm1 mutant zebrafish embryos.

M137

Inhibition of Endothelial SK/IK Channels Con-tributes to Coronary Vascular Dysfunction in the Type-2-Diabetic Mice

Yuhong Liu1, Guangbin Shi1, Elizabeth Harrington2, Frank Sellke1, Jun Feng1

1Rhode Island Hospital, Alpert Medical School Of Brown University, Providence, United States, 2Ocean State Research Institute, VA Medical Center, Alpert Medical School of Brown University, Providence, USA

• Type-2 diabetes is associated with altered func-tion of coronary endothelial SK/IK channels.

• Inhibition of SK/IK channels contributes to coro-nary vascular dysfunction in the diabetic mice.

• Impaired EDHF-induced coronary microvascular relaxation in the diabetic mice.

M138

Insight into the biological role of PDGF-D

Erika Folestad1, Lars Muhl, Hanna Gladh, Ulf Eriksson1Karolinska Institutet,Dept of Medical Biochemistry and Biophysics, Division of Vascular Biology, Stockholm, Sweden

• Expression and characterization of the Pdgfd knockout mouse

• Vascular expression and function of PDGF-D• NRP1 acts as a co-receptor in PDGF-D signaling

M139

Epigenetic activation of pro-angiogenic sig-naling pathways in human endothelial progen-itors increases angiogenesis and vasculogen-esis

Sylvain Fraineau1, Carmen G. Palii2, Brian McNeill3, Morten Ritso2, William C. Shelley4, Nutan Prasain4, Alphonse Chu2, Elodie Vion2, Kristy Rieck2, Sharmin Nilufar2, Theodore J. Perkins2, Michael A. Rudnicki2, David S. Allan2, Mervin C. Yoder4, Erik J. Suuronen3, Marjorie Brand2

1Inserm U1096, Institute for Research and Innovation in Biomedicine, Department of Pharmacology, Normandy University and University of Rouen, Rouen, France, 2Sprott Center for Stem Cell Research, Regenerative Medicine Program, Ottawa Hospital Research Institute, Ottawa, Canada, 3Division of Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, Canada, 4Department of Pediatrics, Indiana University School of Medicine, Indianapolis, USA

• The epigenetic drug combination of deacetylase inhibitor panobinostat and histone H3 lysine 27 trimethyl transferase inhibitor GSK-343 enhances ECFC functions and vascular repair

• The epigenetic drug combination increases the expression of bivalent genes to enhance ECFC functions

• histone acetyl transferase P300 and histone H3 lysine 27 trimethyl demethylase UTX are required for epigenetic drugs effect

M140

Junctional forces and wall shear stress com-pete to coordinate collective endothelial cell polarity

Claudio A. Franco1

1Instituto de Medicina Molecular, Lisbon, Portugal

• Wnt5a/ROR2/Cdc42 promotes junctional tension• Wnt5a positively regulates collective cell migra-

tion at the vascular sprouting front• Junctional tension and shear stress interact to

promote coordinate endothelial polarity

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IVBM2018

M141

Molecular and functional analysis of PDGF signaling in ischemic stroke

Manuel Zeitelhofer1, Christina Stefanitsch1, Ulf Eriksson1, Linda Fredriksson1

1Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden

• Increased signaling by PDGF-CC/PDGFR-alpha in the brain during ischemic stroke augments brain injury

• Blocking PDGF-CC/PDGFR-alpha signaling is safe and improves neurological outcome in human patients suffering ischemic stroke

• Monoclonal anti-PDGF-CC antibody treatment may prove to have superior efficacy and less side effects than PDGFR antagonism using imatinib

M142

Matrix stiffness controls lymphangiogenic growth factor responsiveness and lymphatic vessel formation via GATA2-regulated tran-scriptional programme

Maike Frye1, Andrea Taddei2, Cathrin Dierkes3, Ines Martinez-Corral1, Matthew Matthew Fielden4, Henrik Ortsäter1, Jan Kazenwadel5, Dinis Calado2, Pia Ostergaard6, Marjo Salminen7, Liqun He8, Natasha Harvey5, Friedmann Kiefer3,9, Taija Mäkinen1

1Department of Immunology, Genetics and Pathology, University of Uppsala, Uppsala, Sweden, 2The Francis Crick Institute, London, UK, 3Max Planck Institute for Molecular Biomedicine, Muenster, Germany, 4KTH Royal Institute of Technology, Albanova, Stockholm, Sweden, 5Centre for Cancer Biology, University of South Australia , Adalaide , Australia, 6St George’s University of London, London, UK, 7Department of Veterinary Biosciences, University of Helsinki, Helsinki, Finland , 8Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China , 9European Institute for Molecular Imaging (EIMI), University of Muenster, Muenster, Germany

• Matrix stiffness fundamentally controls lymphatic vascular morphogenesis.

• Venous LEC progenitors experience a decrease in substrate stiffness upon migration out of the cardinal vein, which induces a GATA2-dependent transcriptional program required to form the first lymphatic vessels.

• An increase of GATA2 expression on soft matrix initiates GATA2-dependent upregulation of genes involved in cell migration and lymphangiogenesis.

M143

Guidance cues for the hindbrain central arter-ies during zebrafish development

Mr. Naoki Hirano1, Mr. Hayato Endo2, Misato Fujita1

1Kanagawa University, Hiratsuka, Japan, 2Toyo University, Itakura, Japan

• Candidate genes for guidance cues involved in the hindbrain central arteries formation were selected by exploring expression database.

• The hindbrain central arteries in the candi-date-depleted embryo revealed abnormal pat-terning.

• rfng and scube2, play important roles during pat-terning of hindbrain vessels.

M144

Rap1b regulates hematopoietic stem cell development by promoting Notch signal-me-diated specification of hemogenic endothe-lium

Seung-Sik Rho1, Isao Kobayashi2, Koji Ando3, Eri Oguri1, Naoki Mochizuki3, Shigetomo Fukuhara1

1Inst. of Adv. Med. Sci., Nippon Medical School, Kawasaki, Japan, 2Institute of Science and Engineering, Kanazawa University, Kanazawa, Japan, 3Department of Cell Biology, NCVC, Suita, Japan

• Rap1b is dispensable for vascular development and maintenance of vascular integrity in zebraf-ish.

• Rap1b is involved in hematopoietic stem cell development in zebrafish.

• Rap1b regulates hematopoietic stem cell devel-opment by promoting Notch signal-mediated specification of hemogenic endothelium

M145

Tip cell behavior is regulated by transcrip-tional factor FoxO1 under hypoxic condition.

Moe Fukumoto1, Kanako Kondo1, Kazumasa Uni1, Shinobu Inagaki1, Tatsuo Furuyama2

1Group of Neurobiology, Division of Health Science, Osaka University Graduate School of Medicine, Suita, Japan, 2Kagawa Prefectural University of Health Sciences, Takamatsu, Japan

• Transcription factor FoxO1 accumulates in tip cell nuclei during angiogenesis.

• Hypoxic stimuli induce FoxO1 nuclear accumula-tion in cultured endothelial cells.

• Tip-cell-specific gene esm1 up regulated under hypoxia in FoxO1 dependent manner

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IVBM2018

M146

Nox5 regulates VSMC phenotype switching and extracellular vesicle-mediated calcifica-tion

Gosia Furmanik1, Martijn Chatrou1, Rick van Gorp1, Brecht Willems1, Harald Schmidt2, Alexander Kapustin3, Guillaume van Eys4, Marie-Luce Bochaton-Piallat5, Diane Proudfoot6, Erik Biessen7, Cathy Shanahan3, Chris Reutelingsperger1, Leon Schurgers1

1Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands, 2Department of Pharmacology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands, 3British Heart Foundation Centre of Excellence, Cardiovascular Division, King’s College London, London, United Kingdom, 4Department of Molecular Cell Biology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands, 5Departments of Pathology and Immunology, University of Geneva-CMU, Geneva, Switzerland, 6Signalling ISP, Babraham Institute, Cambridge, United Kingdom, 7Department of Pathology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, Netherlands

• In pathological vascular conditions (e.g. ath-erosclerosis and vascular calcification) vascular smooth muscle cells (VSMCs) change phenotype from contractile to synthetic.

• The synthetic phenotype is associated with increased calcification propensity, extracellular vesicle (EV) release and increased Ca2+-depen-dent NADPH oxidase Nox5 expression.

• Overexpression of Nox5 results in phenotype switching to synthetic, increased oxidative stress and EV release, leading to increased calcification.

M147

Defective endothelial cell migration in the absence of Cdc42 leads to capillary-venous malformations

Bàrbara Laviña1, Mr. Marco Castro1, Colin Niaudet1, Bert Cruys2,3, Peter Carmeliet2,3, Katie Bentley1,4, Cord Brakebusch5, Christer Betsholtz1,6, Konstantin Gaengel1

1Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, , Uppsala, Sweden, 2Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, Leuven, Belgium, 3Laboratory of Angiogenesis and Vascular Metabolism, Vesalius Research Center, VIB, Leuven, Belgium, 4Computational Biology Laboratory, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, , Boston, USA, 5BRIC, University of Copenhagen, Copenhagen, Denmark, 6Integrated Cardio Metabolic Centre (ICMC), Karolinska Institute, , Stockholm, Sweden

• Cdc42 is required for endothelial tip cell selec-tion, directed cell migration, filopodia formation and front-rear polarization.

• Cdc42 is dispensable for apical basal polariza-tion, lumen formation and proliferation of retinal blood vessels.

• Defective cell migration in the absence of Cdc42 prevents normal EC re-distribution and causes capillary-venous malformations.

M148

Role of stearoyl-CoA desaturase in hypox-ia-induced myocardial angiogenesis

Ana-Maria Gan1, Paulina Pawelec1, Adam Olichwier1, Anna Filip1, Sabina Tabaczar1, Victor Navrulin1, Pawel Dobrzyn1

1Nencki Institute Of Experimental Biology, Polish Academy of Science, Warsaw, Poland

• stearoyl-CoA desaturase 4 (SCD4) deficiency decreases fatty acid oxidation after myocardial infarction

• expression of angiogenic factors is altered in SCD4-/- mice in comparison with WT mice after myocardial infarction

• angiogenic process in infarcted heart is strongly linked with stearoyl-CoA desaturase activity

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IVBM2018

M149

Heart of the matter: formation of the zebrafish cardiac lymphatic vasculature in health and disease

Dana Gancz1, Gal Perlmoter1, Ruben Marin Juez2, Didier Stainier2, Karina Yaniv1

1Weizmann Institute Of Science, Rehovot, Israel, 2Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany

• In contrast to the trunk lymphatic vasculature, which develops during early embryogene-sis, zebrafish cardiac lymphatics form at juve-nile-adult stages.

• We distinguish four populations of cardiac lym-phatics, which differ in their origins, morpholo-gies and molecular signatures.

• We detect significant differences in the origins, timing, and mechanisms of formation of different lymphatics in response to injury.

M150

A novel role of Sphingosine-1-phosphate receptor 1 (S1PR1) in embryonic hematopoi-esis

Maria Garcia-Collado1, Christer Betsholtz1, Konstantin Gaengel1

1Uppsala University IGP, Uppsala, Sweden

• Severe liver hypoplasia is a previously overlooked consequence of global S1pr1 deletion.

• S1pr1 deletion leads to a reduction of c-kit+ hematopoietic progenitors.

• S1pr1 might control hematovascular differentia-tion.

M151

The RNA editor, ADAR2, is required for leuko-cyte trafficking to inflamed tissues

Aikaterini Gatsiou1,2,3, Carolin Amrhein1, Almudena Ortega-Gomez4,5, Dinesh K. A. Ramadurai8, Stefan Guenther3,7, Wei Chen9,10, Tommy Regen11, Domenico Alessandro Silvestris12, Shin Kwak13, Craig H. Selzman14,15, Angela Gallo12, Ari Waisman11, Andreas M. Zeiher2,3, Thomas Braun3,7, Stavros Drakos8,15, Oliver Soehnlein4,5,6, Stefanie Dimmeler1,3, Konstantinos Stellos1,2,3,16,17

1Institute of Cardiovascular Regeneration, Center of Molecular Medicine, JW Goethe University Frankfurt, Frankfurt am Main, Germany, 2Department of Cardiology, Center of Internal Medicine, JW Goethe University Frankfurt, Frankfurt am Main, Germany, 3German Center of Cardiovascular Research (Deutsches Zentrum für Herz-Kreislauf-Forschung, DZHK), , Rhein-Main Partner Site, Germany, 4Institute for Cardiovascular Prevention, LMU Munich, Munich, Germany, 5German Center of Cardiovascular Research (Deutsches Zentrum für Herz-Kreislauf-Forschung, DZHK), , Munich Heart Alliance Partner Site, Germany, 6Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden, 7Max-Planck Institute for Heart and Lung Research, Bad Nauheim, Germany, 8Division of Cardiovascular Medicine, University of Utah School of Medicine, Salt Lake City, USA, 9Department of Biology, Southern University of Science and Technology, Shenzhen, China, 10Medi-X Institute, SUSTech Academy for Advanced Interdisciplinary Studies, Southern University of Science and Technology, Shenzhen, China, 11Institute for Molecular Medicine, University of Mainz, Mainz, Germany, 12RNA Editing lab, Oncohaematology Dept., Ospedale Pediatrico Bambino Gesù IRCCS, Rome, Italy, 13Department of Neurology, Graduate School of Medicine, University of Tokyo, Tokyo, Japan, 14Division of Cardiothoracic Surgery, University of Utah, Salt Lake City, USA, 15Nora Eccles Harrison Cardiovascular Research and Training Institute (CVRTI), University of Utah, Salt Lake City, USA, 16Cardiovascular Research Centre, Institute of Genetic Medicine, Newcastle University, Newcastle upon Tyne, UK, 17Cardiothoracic Centre, Newcastle upon Tyne Hospitals, NHS Foundation Trust, Newcastle upon Tyne, UK

• ADAR2 is integral for endothelial cell pro-inflam-matory responses in vitro and in vivo.

• Endothelial ADAR2 controls leukocyte rolling, adhesion and transmigration to inflamed tissues.

• ADAR2-induced adenosine to inosine RNA edit-ing of primary microRNAs comprise a novel post-transcriptional regulatory mechanism of inflammation.

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IVBM2018

M152

The homeobox transcription factor HHEX is an upstream regulator of the VEGFC/FLT4/PROX1 signaling axis

Sébastien Gauvrit1, Alethia Villasenor1, Boris Strilic2, Philip Kitchen3, Michelle M Collins1, Rubén Marín-Juez1, Stefan Guenther4, Hans-Martin Maischein1, Nana Fukuda1, Maurice A Canham5, Joshua M Brickman6, Clifford W Bogue7, Padma-Sheela Jayaraman3, Didier Y R Stainier1

1Department of Developmental Genetics, Max Planck Institute for Heart and Lung Research , Bad Nauheim, Germany, 2Department of Pharmacology, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany, 3Institute of Cancer and Genomic Sciences, University of Birmingham, Birmingham, UK, 4ECCPS Bioinformatics and deep sequencing platform, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany, 5Institute for Stem Cell Research, MRC Centre for Regenerative Medicine, School of Biological Sciences, Edinburgh, UK, 6The Danish Stem Cell Centre (DanStem), University of Copenhagen, Copenhagen, Denmark, 7Department of Pediatrics, Yale University School of Medicine, New Haven, USA

• zebrafish hhex mutants lack sprouting angiogene-sis from the posterior cardinal vein due to defect in the Vegfc/Flt4/Prox1 pathway.

• Tissue-specific genetic deletions in mice reveal its highly conserved function during vascular and lymphatic development.

• HHEX regulates the VEGFC/FLT4/PROX1 pathway in human endothelial cells and directly binds the PROX1 promoter.

M154

The effect of dual purinoreceptor- dependent approach on functioning of Human Microvas-cular Edothelial Cells (HMEC-1)

Anna Gdula1, Anna Selmi1, Marta Stasiak1, Maria Świątkowska1

1Department of Cytobiology and Proteomics, Medical University of Łódź, Łódź, Poland

• The study was intended to investigate the effect of dual purinoreceptor-dependent antiplatelet strategy on the endothelial cells condition.

• Simultaneously, P1 and P2Y-receptors were acti-vated and inhibited respectively. Afterwards, analysis: PrestoBlue, ELISA(VEGF levels), cellular functional tests were carried out.

• Conducted experiments demonstrated a signif-icant change between strategies and confirmed the positive effects of dual antiplatelet therapy on endothelial cells.

M155

Tumor endothelial up-regulation of IDO1 in response to CD40-stimulating immunotherapy

Maria Georganaki1, Alexandros Karampatzakis2, Sander Tuit3, Grammatiki Fotaki1, Luuk van Hooren1, Hua Huang1, Roberta Lugano1, Aura Kaunisto4, Peter Ellmark5, Sara Mangsbo6,7, Joachim Schultze3, Magnus Essand1, Anna Dimberg1

1Department of Immunology, Genetics and Pathology, The Rudbeck Laboratory, Uppsala University, Uppsala, Sweden, 2Manchester Collaborative Centre for Inflammation Research, University of Manchester, Manchester, UK, 3Genomics & Immunoregulation, Life and Medical Science Institute, University of Bonn, Bonn, Germany, 4Novo Nordisk A/S, Copenhagen , Denmark, 5Alligator Bioscience, Lund, Sweden, 6Department of Pharmaceutical Biosciences, Science for Life Laboratory, Uppsala University, Uppsala, Sweden, 7Immuneed AB, Uppsala, Sweden

• RNA-sequencing analysis of tumor endothelial cells isolated from murine tumors treated with CD40-stimulating immunotherapy.

• Increased interferon-γ signaling in the tumor microenvironment after CD40-stimulating immu-notherapy tilts tumor endothelial cells towards an immunosuppressive state by up-regulating IDO1.

• Combining CD40 mAb therapy with the IDO1 inhibitor epacadostat delayed tumor growth and increased survival, correlating with increased activation of cytotoxic T-cells.

M156

AMPK negatively regulates tensin-dependent integrin activity

Maria Georgiadou1, Johanna Lilja1, Guillaume Jacquemet1, Camilo Guzman1, Maria Rafaeva1, Charlotte Alibert2, Yan Yan3, Pranshu Sahgal1, Martina Lerche1, Jear-Baptiste Manneville2, Tomi Mäkelä3, Johanna Ivaska1

1University of Turku, , Finland, 2Institute Curie, Paris, France, 3University of Helsinki, , Finland

• The major metabolic sensor AMPK negatively regulates beta1-integrin activity and integrin-de-pendent processes such as cell adhesion, matrix remodelling and traction force

• Loss of AMPK upregulates the expression of the fibrillar adhesion proteins tensin1 and tensin3

• Tensins enhance integrin activity in fibrillar adhe-sions, fibronectin remodeling and traction stress

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IVBM2018

M157

Csk strengthens endothelial barrier functions partially via VE-cadherin tyrosine 685

Rebekka Gerschütz1, Kathleen Spring1, Ilse Timmerman1, Kerstin Schäfer1, Silke Currie1, Birgit Kempe1, Malte Stasch1, Stefan Volkery1, Astrid Nottebaum1, Dietmar Vestweber1

1Max Planck Institute For Molecular Biomedicine, Münster, Germany

• Csk regulates VE-cadherin Y685 phosphorylation through its ability to inhibit Src activity at endo-thelial junctions.

• Csk is implicated in regulating leukocyte trans-migration in vitro via Cortactin activation and ICAM-1 recruitment to sites of adherent leuko-cytes.

• Increased permeability observed in the absence of Csk is partially mediated by VE-cadherin Y685.

M158

Vascular remodeling in the zebrafish trunk, a story of fate and force

Ilse Geudens1,2, Baptiste Coxam3,4, Véronique Gebala3,4, Silvanus Alt3,4, Anne-Clémence Vion3,4, Holger Gerhardt1,2,3,4,5

1Vascular Patterning Laboratory, Center for Cancer Biology, VIB, Leuven, Belgium, 2Vascular Patterning Laboratory, Vesalius Research Center, Department of Oncology, KU Leuven, Leuven, Belgium, 3Integrative Vascular Biology Lab, Max-Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany, 4DZHK (German Center for Cardiovascular Research), partner site Berlin, Berlin, Germany, 5Berlin Institute of Health (BIH), Berlin, Germany

• during vascular remodeling in the zebrafish trunk transient perfused shunts are formed between the intersomitic blood vessels and secondary venous sprouts

• shunts are resolved depending on directional movement of endothelial cells within the interso-mitic vessels

• directional movement is instructed by a dual mechanism: preprogrammed behavior and flow-mediated reprogramming, together result-ing in formation of a balanced artery-vein net-work

M159

Lateral Induction of Dll4 Expression Initiates non Sprouting Angiogenesis by VEGF

Roberto Gianni Barrera1, Andrea Uccelli1, Marianna Trani1, Elena Groppa1, Raquel Agudo Blanco2, Katie Bentley3, Holger Gerhardt4, Andrea Banfi1

1Department Of Biomedicine And Of Surgery, Basel University Hospital, Switzerland, , Switzerland, 2Vascular biology laboratory, London Research Institute, London, United Kingdom, 3Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Usa, 4Max-Delbrück Center for Molecular Medicine, Helmholtz Association, , Germany

• VEGF determines vascular enlargement and intussusception by activating the Dll4/Notch1 axis in a spatially continuous and stable pattern

• The simultaneous Dll4 expression and Notch1 activation in adjacent ECs is sustained by a mech-anism of lateral induction

• In the setting of therapeutic VEGF delivery and intussusceptive angiogenesis, Notch inhibition increases both vascular growth and functional perfusion

M160

Neuronal guidance cues important for mono-cyte-endothelial cell interaction

Dianne Vreeken1, Caroline Bruikman2, Huayu Zhang1, Wendy Sol1, Anton Jan Van Zonneveld1, Kees Hovingh2, Janine Van Gils1

1Leiden University Medical Center, Leiden, Netherlands, 2Academic Medical Center, Amsterdam, Netherlands

• Concurrent expression changes of neuroimmune guidance cue ligand-receptor combinations upon pro-inflammatory stimulation of endothelial cells and monocytes.

• Inflammatory stimulation significantly down-regulates the endothelial semaphorin receptor PLXNA4, and silencing of PLXNA4 results in endo-thelial barrier loss.

• Reducing monocyte expression of the inflamma-tory responsive EPHB2 receptor results in a vast reduction of monocyte adhesion.

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IVBM2018

M162

APLN/APLNR-targeting improves anti-angio-genic efficiency and blunts pro-invasive side effects of VEGFA/VEGFR2-blockade in GBM

Giorgia Mastrella1, Mengzhuo Hou1, Veit Stöcklein1, Min Li1, Rolf Bjerkvig2, Dolores Hambardzumyan3, Roland Kälin1, Rainer Glass1

1Ludwig Maximilians University, Munich, Germany, 2Department of Biomedicine, University of Bergen, Bergen, Norway, 3Department of Pediatrics and Aflac Cancer Center of Children’s Health Care of Atlanta, Emory University School of Medicine, Atlanta, USA

• Bevacizumab-treatment or VEGFR2-inhibition reduces intratumoral Apelin-levels in gliomas.

• Reduced Apelin-levels blunt angiogenesis but promote tumour-invasion.

• The competitive agonist APLN-F13A inhibits angiogenesis and blocks invasion (alone and syn-ergistically with VEGFR2-blockade).

M163

New pericytes in the adult brain originate from a previously unrecognized pericyte precursor

Rainer Glass1, Roland Kälin1, Yuping Li1, Yingxi Wu1, Verdon Taylor2, Michael Synowitz3, Wolfgang Enard4, Eloi Montanez5

1 Ludwig Maximilians University, Neurosurgical Research, Munich, Germany, 2 University of Basel, Department of Biomedicine, Basel, Switzerland, 3University Hospital Center Schleswig Holstein, Department of Neurosurgery , Kiel, Germany, 4Ludwig Maximilians University, Anthropology and Human Genomics, Munich, Germany, 5Ludwig Maximilians University, Walter-Brendel-Centre of Experimental Medicine, Munich, Geramny

• Pericytes in the adult brain or developing retina derive from non-hematopoietic, avascular, peri-cyte marker-negative cells (pericyte precursors).

• scRNAseq revealed that pericyte precursors are distinct from endothelia, mature vascular mural cells, glia or neurons.

• Pericyte precursors are quiescent in the healthy CNS and become proliferatively activated e.g. during neoplastic angiogenesis, where they rep-resent an excellent therapeutic target.

M164

Micro-RNAs are major players of neutro-phil-endothelium crosstalks in ANCA-associ-ated vasculitis

M. Alexandre Glémain1,2, Mélanie Néel1,2, Rozenn Le Bloas1,2, Fadi Fakhouri1,2, Sarah Bruneau1,2

1Centre De Recherche En Transplantation Et Immunologie UMR1064, INSERM, Université de Nantes, Nantes, France, 2Institut de Transplantation Urologie Néphrologie (ITUN), CHU Nantes, Nantes, France

• Activated neutrophils release extracellular vesi-cles that carry miR-223, miR-142-3p and miR-451 and that target microvascular endothelial cells during ANCA-associated vasculitis.

• miR-142-3p and miR-451 induce endothelial damage and inhibit vascular repair.

• miR-451 induces the activation of EC and triggers a pro-inflammatory environment.

M165

Histone modification H3K4me2 controls Smooth Muscle Cell lineage determination and maintenance in a contractile phenotype

Sidney Mahan1, Anh T. Nguyen2, Gary K. Owens2, Delphine Gomez1

1University Of Pittsburgh, Pittsburgh, United States, 2University of Virginia, Charlottesville, United States

• Enrichment of the histone modification H3K4me2 on the SMC marker genes is an early step during SMC differentiation preceding expression.

• H3K4me2 enrichment on the SMC marker genes is required for their expression in vitro and in vivo.

• First functional epigenetic study showing the H3K4me2 is an essential mechanism of mainte-nance of the SMC contractile phenotype.

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IVBM2018

M166

Predetermined or free will? Is acquired can-cer therapy resistance initiated by the tumour endothelial stroma?

Jesus Gomez Escudero1, Kairbaan Hodivala-Dilke1

1Barts Cancer Institute- Queen Mary University Of London, London, United Kingdom

• Cancer• Endothelial stroma• Drug Resistance

M167

Human blood platelets release a plenitude of endogenous and exogenous cardiovascular disease-related biomarkers upon activation

Knut Fälker1, Magnus Grenegård1

1Cardiovascular Research Centre (CVRC), School of Medical Sciences, Örebro University, 70182 Örebro, Sweden

• Human platelets are known take up and accumu-late proteins from the surrounding plasma.

• We found that platelets release multiple endog-enous and exogenous cardiovascular disease (CVD)-related biomarkers upon activation.

• Platelets may, therefore, provide an easily acces-sible platform for the diagnostics of the develop-ment or stages of CVDs.

M168

Lymphatic endothelium stimulates melanoma metastasis and invasion via MMP14 depen-dent Notch3 and beta1-integrin activation

Pirita Pekkonen1, Sanni E. Alve1, Giuseppe Balistreri1, Silvia Gramolelli1, Olga Tatti-Bugaeva2, Ilkka Paatero3, Otso Niiranen1, Krista Tuohinto1, Nina Perälä1, Adewale Taiwo1, Nadezhda Zinovkina1, Pauliina Repo2, Katherine Icay2, Johanna Ivaska3,4, Pipsa Saharinen1,5, Sampsa Hautaniemi2, Kaisa Lehti2,6,7, Päivi M. Ojala1,7,8

1Research Programs Unit, Translational Cancer Biology, University Of Helsinki, Helsinki, Finland, 2Research Programs Unit, Genome-Scale Biology, University of Helsinki, Helsinki, Finland, 3Turku Centre for Biotechnology, University of Turku, Turku, Finland, 4Department of Biochemistry, University of Turku, Turku, Finland, 5Wihuri Research Institute, Helsinki, Finland, 6Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden, 7Foundation for the Finnish Cancer Institute, Helsinki, Finland, 8Section of Virology, Division of Infectious Diseases, Department of Medicine, Imperial College London, London, United Kingdom

• Melanoma cell crosstalk with lymphatic endothe-lial cells (LECs) enhances metastatic dissemina-tion in vivo.

• MMP14 positively regulates Notch3 and active b1-integrin, both needed for the invasively sprouting cell phenotype of melanoma cells.

• Notch3 and MMP14 are required for melanoma cell metastasis in a zebrafish xenograft model.

M169

Prox1 negatively regulates MMP14 transcrip-tion in cancer and endothelial cells

Silvia Gramolelli1, Jianpin Cheng2, Ines Martinez-Corral3, Markus Vähä-Koskela1, Endrit Elbasani1, Elisa Kaivanto1, Ville Rantanen1, Krista Tuohinto1, Sampsa Hautaniemi1, Mark Bower4, Caj Haglund1,5, Kari Alitalo1, Taija Mäkinen3, Tatiana V. Petrova2, Kaisa Lehti1, Päivi M. Ojala1,6,7

1University Of Helsinki, Helsinki, Finland, 2CHUV and University of Lausanne, Lausanne, Switzerland, 3Uppsala University, Uppsala, Sweden, 4Chelsea and Westminster Hospital and Imperial College London, London, UK, 5Helsinki University Hospital, Helsinki, Finland, 6Imperial College London, London, UK, 7Foundation for the Finnish Cancer Institute, Helsinki, Finland

• Prox1 binds to the MMP14 promoter thereby suppressing its expression.

• Prox1 depletion increased MMP14 expression in murine lymphatic vessels, in human primary cells and cancer cell lines, thus enhancing MMP14-de-pendent 3D-invasiveness.

• Prox1 ectopic expression impairs the MMP14-de-pendent umbilical vein endothelial cell sprouting and metastatic breast cancer cell invasiveness.

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IVBM2018

M170

Antibody blockade of LRG1 normalizes tumor vasculature and enhances the utility of cancer therapeutics

John Greenwood1, Marie O’Connor1, David Kallenberg1, Rene-Filip Jackstadt2, Angharad Watson3, Julia Ohme3, Laura Dowsett1, Jestin George1, Xiaomeng Wang1, Ann Ager3, Owen Sansom2, Stephen Moss1

1University College London, London, United Kingdom, 2Cancer Research UK Beatson Institute, Glasgow, United Kingdom, 3Cardiff University, Cardiff, United Kingdom

• Knockout or antibody inhibition of LRG1 reduces tumour size and increases survival rate in mouse models of cancer.

• Loss or inhibition of LRG1 results in improved tumor vascular pericyte-endothelial cell associ-ation, enhanced perfusion and reduced hypoxia.

• Antibody inhibition of LRG1 enhances signifi-cantly the efficacy of cytotoxic and adoptive T cell therapies.

M171

Noninvasive monitoring of blood flow parame-ters of PDT-treated microvessels

Tatyana Grishacheva1, Dinara Faizullina1, Nickolay Petrishchev1, Irina Mikhailova1, Aleksandr Krivchenko2

1Pavlov First Saint Petersburg State Medical University, Saint Petersburg, Russian Federation, 2Sechenov institute of evolutionary physiology and biochemistry, Saint Petersburg, Russian Federation

• The goal of research was to study the effect of the photodynamic therapy with photosensitizers of different chemical structures on the microvas-culation.

• Studied photosensitizers: chlorin e6 derivative - Radachlorin 5 mg/kg; Coproporphyrin 10 mg/kg; Bengal pink 17 mg/kg.

• The most pronounced effect of endothelium disfunction followed by rapid decrease of mean blood velocity was observed in experiments with Radachlorin.

M172

S-nitrosylation of NOX4 protects Nrf2 defi-cient endothelial cells from oxidative damage and apoptosis

Aleksandra Kopacz1, Damian Kloska1, Dominik Cysewski2, Bartosz Proniewski3, Nicolas Personic1, Aleksandra Piechota-Polanczyk1, Patrycja Kaczara3, Agnieszka Zakrzewska3, Jozef Dulak1, Alicja Jozkowicz1, Anna Grochot-Przeczek1

1Department of Medical Biotechnology, Faculty of Biochemistry Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland, 2Mass Spectrometry Laboratory, Institute of Biochemistry and Biophysics, Polish Academy of Science, Warsaw, Poland, 3Jagiellonian Centre for Experimental Therapeutics, Jagiellonian University, Krakow, Poland

• Although a primary role for Nrf2 transcription factor is protection from oxidative stress, Nrf2 deficient ECs maintain oxidative balance.

• Protection from oxidative damage in ECs lacking Nrf2 is achieved due to S-nitrosylation of NOX4.

• Aggravation of protein S-nitrosylation redirects Nrf2 deficient ECs from apoptosis to senescence, the latter spreads in aortic cells paracrinally.

M173

Microenvironment of proliferative diabetic retinopathy supports lymphatic neovascular-ization

Erika Gucciardo1, Sirpa Loukovaara2, Ani Korhonen1, Pauliina Repo1, Beatriz Martins1, Helena Vihinen3, Eija Jokitalo3, Kaisa Lehti1,4

1Research Programs Unit, Genome-Scale Biology, University of Helsinki, Helsinki, Finland, 2Unit of Vitreoretinal Surgery, Ophthalmology, University of Helsinki and Helsinki University Hospital, Helsinki, Finland, 3Electron Microscopy Unit, Institute of Biotechnology, University of Helsinki, Helsinki, Finland, 4Department of Microbiology, Tumor, and Cell Biology (MTC), Karolinska Institutet, Stockholm SE-17165, Sweden

• Proliferative diabetic retinopathy (PDR) is a major diabetic microvascular complication character-ized by pathological angiogenesis, in need of new translational models.

• By utilizing patient-derived neovascular tissue specimen, we developed a novel clinically rel-evant ex vivo PDR model recapitulating human PDR pathophysiology.

• The ischemia- and inflammation-induced PDR microenvironment supports pathological neolymphvascularization, bringing a new concept to the PDR mechanisms and targeting options.

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IVBM2018

M174

Characterisation of Oncogene-Induced Senescence in Endothelial Colony Forming Cells

Jasenka Guduric-Fuchs1, Miss Aileen Burke1, Edoardo Pedrini Pedrini1, Reinhold Medina1

1Queens’s University Belfast, Belfaast, United Kingdom

• Lentiviral transduction of the mutated (G12V) H-Ras leads to a senescence phenotype in endo-thelial colony forming cells (ECFCs).

• Oncogene-induced senescent ECFCs acquired enlarged flat morphology, underwent cell cycle arrest and were positive for senescence associ-ated β-gal.

• Senescent ECFCs showed a significant downreg-ulation of cyclin proteins and upregulation of senescence markers including a senescent asso-ciated secretory phenotype.

M175

Therapeutic effects of rosuvastatin in hyper-cholesterolemic prediabetic mice in the absence of low-density lipoprotein receptor

Erika Gurzeler1, Anssi Laine1, Teemu Valkama1, Einari Aavik1, Henri Niskanen1, Jenni Huusko1, Minna Kaikkonen1, Seppo Ylä-Herttuala1,2,3

1A.I. Virtanen Institute for Molecular Sciences, University Of Eastern Finland, Kuopio, Finland, 2Gene Threapy Unit, Kuopio University Hospital, Kuopio, Finland, 3Heart Center, Kuopio University Hospital, Kuopio, Finland

• We studied the effects of rosuvastatin in cardio-vascular and diabetic phenotype using a hyperlip-idemic prediabetic mouse model lacking LDLR.

• Rosuvastatin treatment was effective in reducing plasma cholesterol and liver steatosis while hav-ing no deleterious effects on glucose metabolism.

• RNA sequencing showed the specificity of rosu-vastatin at the transcriptional level in the mouse liver.

M177

GDF15 secretion by endothelial progenitor cells improves their functionality but induces an oxidative stress

Guillaume Ha1,2, Nassim Arouche1, Alejandra Vargas-Valderrama1,3, Segolene Ferratge4, Adrienne Anginot1, Georges Uzan1

1UMRS-MD 1197, Villejuif, France, 2Université Paris Diderot, Paris, France, 3Université Paris Sud. Université Paris-Saclay, Orsay, France, 4Cellenion, Lyon, France

• There is an higher expression of oxidative stress markers in AB-EPC than in UCB-EPC

• The stress marker GDF15 is linked to the genera-tion of an oxidative stress in endothelial progen-itor cells

• Addition of GDF15 improves endothelial progeni-tor cells functionality

M178

Retinal angiogenesis is regulated by vascu-lar smooth muscle cells through PI3K/Akt1/Notch3 signaling pathway

Jung Min Ha1, Seo Yeon Jin1, Hye Sun Lee1, Farzaneh Vafaeinik1, Seo Jin Maeng1, Hye Jin Kum1, Yoo Jin Jung1, Sun Sik Bae1

1Pusan National University School Of Medicine, Yangsan-si, South Korea

• Retinal angiogenesis was delayed in retinas from VSMC-specific Akt1 deficient mice.

• Recruitment and coverage of VSMC to endothe-lium were defected in VSMC-specific Akt1 defi-cient mice.

• Retinal endothelial cell proliferation was inhib-ited in retinas from VSMC-specific Akt1 deficient mice.

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IVBM2018

M179

VIPAR, a quantitative diagnostic approach for 3D histopathology applied to lipedematous and lymphedematous tissue

Rene Haegerling1,2, Dominik Drees3, Aaron Scherzinger3, Pia Ostergaard2, Sahar Mansour2, Dietmar Vestweber4, Stefan Butz4, Xiaoyi Jiang3, Peter S. Mortimer2, Friedemann Kiefer1,5

1Mammalian Cell Signaling Laboratory, Max Planck Institute for Molecular Biomedicine, Muenster, Germany, 2Cardiovascular and Cell Sciences Institute, St. George’s University of London, London, United Kingdom, 3 Pattern Recognition and Image Analysis Group, Department of Computer Science, University of Münster, Muenster, Germany, 4Department of Vascular Cell Biology, Max Planck Institute for Molecular Biomedicine, Muenster, Germany, 5 European Institute for Molecular Imaging, University of Münster, Muenster, Germany

• VIPAR = volume information-based histopatho-logical analysis by 3D reconstruction and data extraction based on light-sheet-imaging.

• VIPAR is a highly reproducible, volume-based tis-sue reconstruction, data extraction and analysis approach that successfully distinguised healthy from pathological skin.

• VIPAR allows identifiction of the underlying vas-cular pathology as well as a more sophisticated phenotyping of patients with blood and lym-phatic vascular diseases.

M180

Targeting b1-integrin inhibits vascular leakage in endotoxemia

Laura Hakanpää1, Elina Kiss1, Guillaume Jacquemet2, Ilkka Miinalainen3, Martina Lerche2, Camilo Guzmán2, Eero Mervaala1, Lauri Eklund3, Johanna Ivaska2, Pipsa Saharinen1

1Helsinki University, Finland, 2University of Turku, Turku, Finland, 3University of Oulu, Oulu, Finland

• b1-integrin promotes endothelial cell contractil-ity and permeability in inflammation

• IL-1b, thrombin and LPS induce the formation of b1-integrin and tensin-1 positive fibrillar adhe-sions that destabilize endothelium in an Angio-poietin-2 dependent manner

• b1-integrin targeting reduces vascular leakage in endotoxemia, providing a novel possibility of vas-cular stabilization in pathological vascular leak

M181

Platelet-induced EMT in Mammary Epithelium Is Dependent on TBK1

Yanyu Zhang1, Ragaseema V Madhavan1, Anahita Hamidi1, Laja Caja1, Falk Saupe1, Agneta Siegbahn1, Aristidis Moustakas1, Associate Anna-Karin Olsson1, Jessica Cedervall1

1Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Uppsala, Sweden

• Platelets induced EMT in mammary epithelial cells.

• TBK1 knock-down suppressed platelet-induced EMT.

• Platelet-induced phosphorylation and nuclear translocation of RelA/p65 was suppressed by TBK1 knock-down.

M182

Development of coronary artery lesions in Kawasaki disease was associated with certain Kawasaki disease-specific molecules

Yasutaka Nakashima2, umi MIzuno1, Kenji Furuno1, Hisanori Nishio2, Yasunari Sakai2, houichi Ohga2, Toshiro Hara1

1Fukuoka Children’s Hospital, Fukuoka , Japan, 2Department of Pediatrics, Kyushu University, Fukuoka, Japan

• We established a new Kawasaki disease (KD) model mouse by oral administration of NOD1 ligand (2011 ATVB) and analyzed the pathophys-iology of NOD1 ligand-induced coronary arteritis (2015 ATVB).

• We searched and identified KD-specific mole-cules, possibly PAMPs/DAMPs, in sera (2014 PLoS ONE).

• We report here that certain KD-specific mole-cules appear to be associated with vasculitis itself in KD.

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IVBM2018

M183

Human adipose stem cells act as pericytes and suppress hyperglycemia-induced pro-in-flammatory activation of retinal EC.

Ghazaleh Hajmousa1, Ewa Przybyt1, Frederick Pfister2, Genaro Parades1, Kondaiah Moganti2, Stephanie Busch2, Jeroen Kuipers3, Klaas Sjollema3, Ingeborg Klaassen4, Hans-Peter Hammes2, Guido Krenning1, Martin C. Harmsen1

1Department of Pathology & Medical Biology, University Medical Center Groningen, Groningen, Netherlands, 25th Medical Department, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, 3Molecular Imaging and Electron Microscopy, Department of Cell Biology, University Medical Center Groningen, Groningen, Netherlands, 4 Department of Ophthalmology, Academic Medical Center, University of Amsterdam, Amsterdam, Netherlands

• Diabetes i.e. hyperglycemia, causes retinal peri-cyte dropout

• ASC can replace lost retinal pericytes• ASC suppress ROS and inflammatory activation of

retinal EC

M184

The role of ELTD1/ADGRL4 in tumour angio-genesis

Koon Ang1, Esther Bridges1, David Favara1, Helen Sheldon1, Demin Li2, Masimo Masiero2, Alison Banham2, Adrian Harris1

1Oncology Department, Oxford University, Oxford, United Kingdom, 2NDCLS, Oxford University, Oxford, United Kingdom

• ELTD1 is highly expressed in the vasculature of human breast cancer metastases and and regu-lates ATP citrate lyase.

• Exosomes from endothelial cells contain extracel-lular ELTD1, which transmits a highly angiogenic signal to recipient endothelial cells.

• Inducible knockdown is far more effective in blocking angiogenesis in vivo and in vitro than constitutive, demonstrating compensatory mech-anisms occur.

M185

Effects of exogenous ouabain on endotheli-um-dependent relaxation

Chunrong HE1, Paul Vanhoutte, Wai Sum Leung1The University Of Hong Kong, Hong Kong, China

• ouabain likely impairs the nitric oxide pathway to reduce endothelium-dependent relaxations;

• When the major mechanisms for the generation of endothelium-derived relaxing signals (namely, nitric oxide, prostanoids and EDH) are inhibited, ouabain unmasks the relaxation to AA which is, to some extent, associated with members of a trian-gle, sodium pumps, nitric oxide and KIR.

M186

Interplay of VEGFRs in regulation of angiogen-esis and vascular permeability

Krista Heinolainen1, Sinem Karaman1, Shentong Fang1, Georgia Zarkada1, Kari Alitalo1

1Wihuri Research Institute And Translational Cancer Biology Program, Helsinki, Finland

• VEGFR1 and VEGFR3 regulate vascular permea-bility and angiogenesis via modulation of VEGF/VEGFR2 signaling.

• VEGFR1 and VEGFR3 are differentially involved in angiogenesis and vascular permeability in differ-ent vascular beds.

• Compound deletion of VEGFR1 and VEGFR3 has revealed an interplay between the different VEG-FRs in the regulation of vascular permeability.

M187

Hypoxia and interaction with macrophages induce characteristics of endothelial-to-mes-enchymal transition observed in atherosclero-sis

Alexandra Helmke1, Janis Casper1, Johannes Nordlohne1, Hermann Haller1, Elisabeth Zeisberg2, Sibylle Von Vietinghoff1

1Hannover Medical School, Germany, 2Universität Göttingen, Germany

• The number of cells with simultaneous expres-sion of endothelial and mesenchymal markers increases in atherosclerosis, indicating endotheli-al-to-mesenchymal-transition (EndMT).

• Interaction with macrophages induces partial EndMT.

• Hypoxia induces an EndMT phenotype similar to what is observed in atherosclerosis in vivo.

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IVBM2018

M188

Calcium Sensing receptors and the regulation of vascular tone

Harry Greenberg1, Anthony Albert1

1St George’s University Of London, London, United Kingdom

• The Calcium Sensing Receptor (CaSR) is a G-pro-tein coupled receptor that senses free extracellu-lar calcium.

• CaSRs are expressed in the vasculature. Endothe-lial calcium sensing receptors regulate vascular tone by causing significant vasorelaxations.

• Calcium sensing receptor induced relaxations occur via nitric oxide synthesis, induced by the opening of TRPV4/C1 ion channels

M189

Vaccination against galectin-1 promotes cytotoxic T-cell infiltration in melanoma and reduces tumor burden

Julia Femel1, Luuk van Hooren2, Melanie Herre1, Falk Saupe1, Elisabeth JM Huijbers1, Danielle RJ Verboogen1, Matthias Reichel1, Jessica Cedervall1, Victor L Thijssen3, Lars Hellman4, Arjan W Griffioen3, Anna Dimberg2, Anna-Karin Olsson1

1Department of Medical Biochemistry and Microbiology, Science for Life Laboratory, Uppsala University, Biomedical Center, Box 582, SE-75123, Uppsala, Sweden, 2Department of Immunology, Genetics and Pathology, Uppsala University, Rudbeck Laboratory, SE-75185 , Uppsala, Sweden, 3Angiogenesis Laboratory, Department of Medical Oncology, Cancer Center Amsterdam (CCA), VU University Medical Center, De Boelelaan 1117, 1081 HV , Amsterdam, The Netherlands, 4Department of Cell and Molecular Biology, Uppsala University, Biomedical Center, Box 596, SE-75124, Uppsala, Sweden

• It is possible to generate high antibody titers against the pro-angiogenic and immunosuppres-sive self-protein galectin-1 by therapeutic vacci-nation.

• Targeting galectin-1 by vaccination significantly decreases melanoma tumor growth in mice.

• Vaccination against galectin-1 improves tumor perfusion and leads to increased infiltration of GrzB+ cytotoxic T cells.

M190

MDR1/ABCB1 upregulation in tumor blood vessels by chemotherapy-induced IL-8

Kyoko Hida1,2, Hiroshi Kikuchi1,3, Nako Maishi1,2, Takashige Abe3, Satoshi Maruyama3, Toru Harabayashi4, Kaname Ameda5, Yoshihiro Matsuno6, Yasuhiro Hida7, Nobuo Shinohara3

1Vascular Biology, Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan, 2Department of Oral Pathology and Biology, Hokkaido University of Graduated School of Dental Medicine, Sapporo, Japan, 3Department of Renal and Genitourinary surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan, 4Dept. Urol., Hokkaido Cancer Ctr., Sapporo, Japan, 5Hokkaido Hinyokika Kinen Hosp., Sapporo, Japan, 6Dept. Surg. Pathol., Hokkaido Univ. Hosp., Sapporo, Japan, 7Dept. Cardiovascular and Thoracic Surg. Grad. Sch. Med., Hokkaido Univ., Sapporo, Japan

• Anti-cancer drugs treatment induced ABC trans-porter upregulation in tumor endothelial cells but not tumor cells.

• The high ratio of ABCB1-positive tumor blood vessels was correlated with poor prognosis.

• IL-8 production -induced by chemotherapy increased ABCB1 expression in tumor endothelial cells.

M191

Biglycan, tumor endothelial cell secreting proteoglycan, as possible biomarker for lung cancer

Yasuhiro Hida1, Hirofumi Morimoto4, Nako Maishi2,3, Hiroshi Nishihara5, Yutaka Hatanaka6, Yoshihiro Matsuno6, Toru Nakamura4, Satoshi Hirano4, Kyoko Hida2,3

1Department of Cardiovascular and Thoracic Surgery, Hokkaido University Graduate School of Medicine , Sapporo, Japan, 2Vascular Biology, Institute for Genetic Medicine, Hokkaido University , Sapporo, Japan, 3Department of Oral Pathology and Biology, Hokkaido University Graduate School of Dental Medicine , Sapporo, Japan, 4Department of Gastroenterological Surgery II, Hokkaido University Graduate school of Medicine, Sapporo, Japan, 5Genomics Unit, Keio Cancer Center, Keio University School of Medicine, Tokyo, Japan, 6 Department of Surgical Pathology, Hokkaido University Hospital, Sapporo, Japan

• We have found that biglycan secreted from tumor endothelial cells, promoted intravasation of tumor cells and lung metastasis in vivo mouse tumors.

• The biglycan positive vessel density in primary lung tumor tissue was significantly correlated with primary and pleural tumor invasion.

• The preoperative serum biglycan level was also significantly correlated with primary tumor inva-sion, pleural invasion.

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IVBM2018

M192

Unbiased screening of S1PR1-signaling mod-ulators by CRISPR-based gene activation system

Yu Hisano1, Eric Engelbrecht1, Mari Kono2, Koki Kawakami3, Asuka Inoue3, Junken Aoki3, Richard Proia2, Timothy Hla1Boston Children’s Hospital, Boston, United States, 2National Institutes of Health, Bethesda, United States, 3Tohoku University, Sendai, Japan

• Screening and identification of S1PR1-modulators by CRISPR-based gene activation system.

• Transactivation of β-arrestin recruitment to S1PR1 by different GPCR,

• Intrinsic ligand independent β-arrestin recruit-ment

M193

Simultaneous deletion of VEGF-B and VEGF-D in hyperlipidaemic mice causes changes in intestinal lipid absorption

Krista Hokkanen1, Annakaisa Tirronen1, Taina Vuorio1, Seppo Ylä-Herttuala1,2

1A. I. Virtanen Institute, University Of Eastern Finland , Kuopio, Finland, 2Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Hyperlipidaemic Ldlr-/-/ApoB100/100 mice defi-cient for both VEGF-B and VEGF-D displayed a delayed intestinal lipid absorption pattern.

• VEGF-B and VEGF-D double knockout mice exhib-ited shorter villi, which resulted in increased rel-ative lacteal length, but reduced absorptive area.

• Lipid staining revealed a tendency of lipids to accumulate around collecting lacteals, suggesting delayed chylomicron secretion to circulation.

M194

The role of endothelial extracellular vesicles in coagulation and cell-cell communication

Wolfgang Holnthoner1, Severin Muehleder1, Heinz Redl1

1Ludwig-Boltzmann-Institute for Experimental and Clinical Traumatology, Vienna, Austria

• Endothelial Cells secrete different extracellular vesicles (EVs): apoptotic bodies, microvesicles and exosomes

• Different methods to isolate and characterize EVs• The role of microvesicles and exosomes in blood

coagulation and angiogenesis

M195

Novel methods for vessel identification and assessment of concurrent dynamic vascular events

Naoki Honkura1, Mark Richards1, Bàrbara Laviña1, Miguel Sáinz-Jaspeado1, Christer Betsholtz1, Lena Claesson-Welsh1

1Dept Immunology, Genetics and Pathology, Rudbeck Laboratory, Uppsala University, , Sweden

• Intravital imaging of vascular dynamic structure and function

• Novel method for identification of vessel types• Vessel type-specific regulation of vascular perme-

ability, vasodilation and flow

M196

Different importance of VE-cadherin for devel-opment and maintenance of specific lym-phatic vessel beds

Esther Hoppe1,4, Rene Hägerling1, Cathrin Dierkes1, Taija Makinen2, Stefan Butz3, Dietmar Vestweber3,5, Friedemann Kiefer1,4,5

1Max Planck Institute for Molecular Biomedicine, Mammalian Cell Signaling Laboratory, Münster, Germany, 2Uppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden, 3Max Planck Institute for Molecular Biomedicine, Department Vascular Cell Biology, Münster, Germany , 4European Institute for Molecular Imaging (EIMI), University of Münster, Münster, Germany , 5DFG Cluster of Excellence 1003 CiM, Münster, Germany, 6Cells in Motion, Germany

• Prenatal deletion of VE-cadherin leads to increased lymphangiogenesis, oedema formation and embryonic lethality.

• In adult mice, the dermal lymphatic vasculature remains largely unaffected by VE-cadherin dele-tion, however neonatal loss results in fragmented lymphatic vessels.

• Mesenteric and intestinal lymphatic vessels are highly affected by VE-cadherin loss, causing frag-mentation and hyperplasia independent of age.

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IVBM2018

M197

A cell sheet-based approach towards artificial blood vessel generation

Anke Hoppensack1, Elisa Lisicki1, Daniel Stoebener1, Johanna Scholz1, Marcus Lindner1, Marie Weinhart1

1Freie Universität Berlin, Institute Of Chemistry And Biochemistry, Germany

• Confluent cell sheets of vascular cell types can be detached temperature-triggered from Poly(glyc-idyl ether)-coated thermoresponsive surfaces

• Tools were developed to roll up detaching cell sheets onto a cylindrical gelatin template that can be removed afterwards

• As a proof-of-principle, tubular structures with an inner layer of EC and outer layers of SMC were generated

M198

RhoB and Cdc42 coordinate the push and pull of endothelial integrity

Peter Hordijk1, Joana Amado-Azevedo1, Manon Pronk1, Jan van Bezu1, Victor van Hinsbergh1, Igor Kovacevic1

1Vumc, Amsterdam, Netherlands

• Endothelial integrity is the net result of barrier stabilizing (push) and barrier disrupting (pull) sig-naling pathways.

• The Cdc42 and RhoB GTPases are central in the signaling towards balanced dynamics of endothe-lial cell-cell contact

• Continuous ubiquitylation of RhoB is required to limit contractilty and stabilize the endothelial barrier.

M199

MPDZ Trafficking Underlies Endothelial Cell Junction Dynamics

Arie Horowitz1

1Thomas Jefferson University, Philadelphia, United States

• Endothelial cell junction transmembrane proteins either undergo trafficking with the modular scaf-fold protein MPDZ or remain separate and anchor it to the junctions.

• The MPDZ-associated GTPase activating protein TBC1D2 prevents junction protein degradation by inhibiting Rab7.

• MPDZ undergoes Rab13-dependent membrane trafficking between the plasma membrane and the trans Golgi network. It is a potential collective coordinator of junction protein dynamics.

M200

The interplay of endothelial-perivascular signaling in FGF-2 induced tumor vascular remodeling

Kayoko Hosaka1, Yunlong Yang1, Masaki Nakamura1, Partrik Andersson1, Xiaojuan Yang1, Yin Zhang1, Takahiro Seki1, Scherzer Martin1, Olivier Dubey1, Xinsheng Wang2, Yihai Cao1

1Karolinska Institute, Stockholm, Sweden, 2The Affiliated Hospital of Qingdao University, Qingdao, , China

• FGF-2 is a potent vascular remodeling fac-tor which stimulates pericyte proliferation and recruitment into tumor vasculatures in vivo through FGFR2.

• FGF-2 sensitizes the PDGFRb signaling through increasing PDGFRb levels in pericytes and enhances pericyte proliferation and migration.

• Under the FGF-2 influence, expression of PDGFR ligands in endothelial cells augmented.

M201

Role of Notch1 in the Angiogenic Potential of Mouse Embryonic Stem Cell-derived Endo-thelial Cells

Tae Wook Lee1, Eun Kyoung Do1, Hye Ji Moon1, Jae Ho Kim1

1Pusan National University School Of Medicine, , South Korea

• Notch1 promotes endothelial maturation and arterial specification during the differentiation of embryonic stem cells to endothelial cells

• Notch1 increases the angiogenic potential of endothelial cells.

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IVBM2018

M202

Markers of microvascular dysfunction are associated with depressive symptoms: the Maastricht Study

Alfons Houben1,2, Marnix van Agtmaal1,2, Ben Sorensen1,2, Tos Berendschot3, Jan Schouten3, Sebastian Kohler4, Nicolaas Schaper1,2, Ronald Henry1,2, Carla van der Kallen1,2, Annemarie Koster5, Simone Eussen6, Miranda Schram1,2, Coen Stehouwer1,2

1Dept. of Internal Medicine; MUMC, Maastricht, Netherlands, 2School for Cardiovascular Disease-CARIM, maastricht, Netherlands, 3dept. of Ophthalmology; MUMC, maastricht, Netherlands, 4dept. of Psychiatry and Neuropsychology; MUMC, maastricht, Netherlands, 5dept. of Social Medicine; MUMC, maastricht, Netherlands, 6dept. of Epidemiology; MUMC, maastricht, Netherlands

• The vascular depression hypothesis suggests that microvascular dysfunction is involved in the etiol-ogy of depression.

• We found, in this population-based cohort study, that markers of microvascular dysfunction in ret-ina, skin, plasma are independently associated with depressive symptoms.

• These findings support the vascular depression hypothesis and might provide a potential target for the prevention and treatment of depression.

M203

Relevance of endothelial and neuronal NOS in the autoregulation of cerebrocortical blood flow in mice

László Hricisák1, Laura Simoes Dobrydnio1, Nikolett Jabronka1, Piroska Portörő-Gál1, Anna Janovicz1, Andreas Polycarpou1,2, Zoltán Benyó1

1Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary, 2Cardiac Surgery Department, Grosshadern Hospital, Ludwig-Maximillian University, Munich, Germany

• nNOS-deficient mice can recover faster after uni-lateral common carotid artery occlusion (CAO) probably due to an upregulated compensatory mechanism

• Pharmacologically blocking all NOS isoforms with L-NAME results in worsening of the recovery in the parietal region after CAO

• NOS plays a role in the cerebrovascular autoreg-ulation after CAO, although the different isoforms can compensate the loss of each other

M204

The soluble epoxide hydrolase attenuates pathological vascularization by preventing astrocyte loss in retinopathy of prematurity

Jiong Hu1,2, Sofia-Iris Bibli1,2, Janina Wittig1, Jihong Lin3, Rüdiger Popp1,2, Hans-Peter Hammes3, Ingrid Fleming1,2

1Institute For Vascular Signalling, Goethe University, Frankfurt, Germany, 2German Centre for Cardiovascular Research (DZHK) partner site Rhein-Main, Frankfurt, Germany, 3Fifth Medical Department, University Medicine Mannheim, University of Heidelberg, Mannheim, Germany

• Ablation of sEH accelerated astrocyte loss and increased pathological neo-vascularization in ret-inas in the mouse model of oxygen-induced reti-nopathy.

• Hyperoxygen attenuated the association of prese-nilin-1 with mitochondrial carrier homolog 1 thus trigged mitochondrial DNA damage and astrocyte apoptosis.

• sEH product 19,20-DHDP suppressed the inte-gration of cholesterol into mitochondrial mem-brane thus protected astrocyte from hyperoxgen induced apoptosis.

M205

Inhibition of the soluble epoxide hydrolase attenuates diabetic retinopathy

Jiong Hu1,2, Sarah Dziumbla1,2, Jihong Lin3, Sofia-Iris Bibli1,2, Sven Zukunft1,2, Kavi Devraj4, Akrit Sodhi5, Stefan Liebner4, Hans-Peter Hammes3, Rüdiger Popp1,2, Ingrid Fleming1,2

1Institute For Vascular Signalling, Centre for Molecular Medicine, Goethe University, Frankfurt am Main, Germany, 2German Centre for Cardiovascular Research (DZHK) partner site RheinMain, Frankfurt am Main, Germany, 35th Medical Department, University Medicine Mannheim, University of Heidelberg, Mannheim, Germany, 4Institute of Neurology (Edinger-Institute), Goethe-University, Frankfurt am Main, Germany, 5Wilmer Eye Institute, Johns Hopkins School of Medicine,, Baltimore, USA

• sEH and its DHA-diol metabolite, 19,20-dihydroxy-docosapentaenoic acid (DHDP), were increased in diabetic retinas in animals and humans.

• 19,20-DHDP targeted cell membranes to alter the localization of cholesterol-binding proteins, and prevented the association of presenilin-1 with N-cadherin and VE-cadherin, thereby compro-mising pericyte–endothelial cell and inter-endo-thelial cell junctions.

• sEH inhibition prevented diabetic retinopathy in Ins2Akita mice.

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IVBM2018

M206

Single Cell Sequencing of Intratumoral High-Endothelial Venules

Marie Duhamel1, Rindert Missiaen1, Yichao Hua1, Gabriele Bergers1,2

1VIB-Center for Cancer Biology, Department of Oncology, Katholieke Universiteit Leuven, Leuven, Belgium, 2Department of Neurological Surgery, Brain Tumor Research Center, Helen Diller Family, Comprehensive Cancer Center, University of California, San Francisco, San Francisco, USA

• Intratumoral HEVs are correlated with improved outcome.

• Combined PDL1 checkpoint inhibitors plus anti-angiogenic agents enhanced T-cell influx and activity in part due to intratumoral HEV forma-tion.

• Single cell transcriptomics of tumor and LN EC and HEV was performed to elucidate intratu-moral HEV ontogeny.

M207

Directing the immune system towards the tumor vasculature by vaccination against extracellular vimentin

Elisabeth J. M. Huijbers1, Judy R. van Beijnum1, Arjan W. Griffioen1

1Angiogenesis Laboratory, Department Of Medical Oncology, Cancer Center Amsterdam, VU University Medical Center, Amsterdam, Netherlands

• Identification of novel tumor endothelial mark-ers,

• Induction of a humoral immune response against the tumor vasculature,

• Vaccination against the tumor vascular marker extracellular vimentin

M208

Gene expression profiling of HUVEC, ECFC-EC and iPS-EC during in vitro vascular morphogenesis

Nan Hultgren1, Christopher Hughes1

1University Of California Irvine, Irvine, United States

• HUVEC, ECFC-EC and iPS-EC differ in their ves-sel-forming abilities.

• RNA-seq indicates that iPS-EC have drastically different gene expression profile comparing to HUVEC and ECFC-EC

• We are developing a list of genes critical for ves-sel formation and a cocktail of growth factors and ECM components to improve iPS-EC function.

M209

AmotL2 is crucial for mechanotransduction, shape and shear-stress resistance of endo-thelial cells

Yuanyuan Zhang1, Sara Hultin1, Evelyn Hutterer1, Sumako Kameishi1, Fabrizio Orsenigo2, Lars Holmgren1

1Department of Oncology and Pathology, Cancer Centrum Karolinska (CCK), Karolinska Institutet, Solna, Stockholm, Sweden, 2FIRC Institute of Molecular Oncology (IFOM), Department of Biological Sciences, School of Sciences, University of Milan, Milan, Italy

• Arterial endothelial cells are able to respond to mechanical forces exerted by fluid shear stress, which is protective against vascular diseases

• The scaffold protein Amotl2 is essential for the cellular shape of endothelial cells by regulating the formation of radial actin filaments

• Deletion of endothelial AmotL2 affects nuclear shape and positioning

M210

Possibility of Taurine complex as an anti-thrombotic agent: In vitro study

Sangho Hyun1, Jonghyun Byun2

1Republic Of Korea Air Force, Chungju-si, South Korea, 2Hanmir Co., Ltd., Seoul, South Korea

• The modified taurine mixed with pentose solu-tions showed statistically longer blood clotting time than aspirin.

• This study was conducted as a preliminary experi-ment to find the combination that shows the best antithrombotic effects, using modified taurine.

• The modified taurine (Patent number: 9877938) shows different characteristics from taurine, and when mixed with pentose, it displays stronger antithrombotic effect.

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IVBM2018

M211

Nf2/Merlin regulates invasive tip cell behavior governing VEGFR2 signaling during angiogen-esis.

Jung Hyun Bae1,2, Yoo Hyung Kim1,2, Jeongwoon Choi1,2, Yoshiaki Kubota3, Gou Young Koh1,2

1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea, 2Center for Vascular Research, Institute for Basic Science (IBS), Daejeon, South Korea, 3Department of Vascular Biology, The Sakaguchi Laboratory, Keio University School of Medicine, Tokyo, Japan

• EC-specific Nf2 deletion from P2 led to hyperplas-tic vascular growth with accompanying filopodial burst in retinal vessel at P6.

• Mechanistically, Nf2/Merlin bound with Angio-motin in contact dependent manner, inhibiting VEGFR2 internalization, and downstream signal-ing in endothelial cell.

• Nf2/Merlin plays critical roles in regulating tip cell behavior by governing VEGFR2 signaling during sprouting angiogenesis.

M212

VEGF-B induces myocardium-specific angio-genesis via regulation of nicotinic acetylcho-line receptors

Olli-Pekka Hätinen1, Johanna Lähteenvuo1, Henna Korpela1, Suvi Jauhiainen1, Antti Kuivanen1, Oscar Liu1, Seppo Ylä-Herttuala1

1A.I.Virtanen Institute for molecular sciences, University of Eastern Finland, Kuopio, Finland

• VEGF-B induces angiogenesis only in myocar-dium.

• VEGF-B upregulates expression of nAChR α4β2 on vascular endothelium of myocardial capillar-ies.

• The angiogenic effect of VEGF-B can be altered with specific nAChR α4β2 agonist and antagonist.

M213

Isolation of endothelial stem cells and their application for regenerative medicine

Tomohiro Iba1, Hisamichi Naito1, Taku Wakabayashi1, Nobuyuki Takakura1

1Osaka University, 3-1 Yamadaoka, Suita, Japan

• We isolated endothelial stem cells from fat, skin and placenta blood vessels.

• These cells can regenerate blood vessels in vivo.• We identified sub-fractions in these cells by singe

cell analysis.

M214

PIK3CA mutation H1047R is associated with angiomatosis of soft tissue

Henna Ilmonen1, Sara Keränen1, Suvi Jauhiainen1, Pia Vuola2, Erkki Tukiainen2, Jouko Lohi3, Kimmo Lappalainen4, Päivi Salminen5, Seppo Ylä-Herttuala1,6,7, Johanna Laakkonen1

1A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland , Kuopio, Suomi, 2Department of Plastic Surgery, Helsinki University Hospital, Helsinki, Finland, 3Department of Pathology, HUSLAB, Helsinki University Hospital, Helsinki, Finland, 4Department of Radiology, HUS Medical Imaging Center, Helsinki University Hospital, Helsinki, Finland, 5Department of Pediatric Surgery, Children’s Hospital, Helsinki University Hospital, Helsinki, Finland, 6Science Service Center, Kuopio University Hospital, Kuopio, Finland, 7Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Angiomatosis of soft tissue (AST) are unclassified benign intramuscular vascular lesions consisting of different-sized vessels and mesenchymal tissue

• PI3K/AKT/mTOR pathway activating PIK3CA p.H1047R mutation was found in 4/10 AST lesions making it the first mutation linked to AST

• Genetic screening is important to differentiate AST patients having PIK3CA mutations as these may be accordingly managed with PI3K/AKT/mTOR inhibitors

Posters – Monday

– 77 –

IVBM2018

M215

Endothelial Gs is involved in flow-dependent vascular tone regulation

Andras Iring1,2, Peter Dancs1,2, Akiko Nakayama1, ShengPeng Wang1, Lee Weinstein3, Stefan Offermanns1,4

1Max-Planck-Institute For Heart and Lung Research, Bad Nauheim, Germany, 2Institute of Clinical Experimental Research, Semmelweis University, Budapest, Hungary, 3National Institutes of Health, Bethesda, USA, 4Centre for Molecular Medicine, University of Frankfurt, Frankfurt am Main, Germany

• Endothelial Gs regulates flow-dependent NO pro-duction

• Loss of endothelial Gs abolish flow-induced vaso-dilatation in isolated arteries

• Absence of endothelial Gs in vivo promotes hypertension

M216

Targeting β-catenin affects in vitro cell survival and ovarian xenograft tumor growth

Sebastián Bocchicchio1, Melanie Ochendrowitsch1, Marta Tesone1, Griselda Irusta1

1Instituto de Biología y Medicina Experimental (CONICET)., Ciudad autónoma de Buenos Aires, Argentina

• Wnt/β-catenin signaling regulates ovarian cancer cell lines proliferation and migration.

• Wnt/β-catenin signaling is involved in ovarian tumor growth.

• Wnt/β-catenin controls ovarian tumor angiogen-esis.

M217

Cre recombination in hematopoietic cells of smooth muscle cell-targeted Cre recombina-tion mice

Tomohiko Ishibashi1, Tadakatsu Inagaki1, Hiroyoshi Mori1, Takeshi Masaki1, Makoto Okazawa1, Yoshikazu Nakaoka1

1Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita, Japan

• Cre expression in myeloid lineage hematopoietic cells of smooth muscle cell (SMC)-targeted Cre recombination mice was reported

• Cre recombination of hematopoietic tissues of SMC-targeted Cre recombination mice were ana-lyzed with flow cytometry

• Lymphoid lineage cells and less differentiated hematopoietic cells showed Cre recombination

M218

Endothelial TGF-β signaling inhibit tumor angiogenesis and metastasis

Fmiko Itoh1, Takahiro Takagi1, Yuki Saito1, Tatsuki Miyamoto1, Toshihiko Inagawa, Yota Nakano2, Kengo Sano2, Marcus Fruttiger3, Susumu Itoh2

1Tokyo University Of Pharmacy And Life Sciences, Hachioji, Japan, 2 Showa Pharmaceutical University,, Machida, Japan, 3UCL Institute of Ophthalmology, London, United Kingdom

• Endothelial specific knockout of TGF-β type II receptor (TβRII) in the postnatal mouse signifi-cantly potentiates tumor angiogenesis in vivo.

• Loss of TβRII inhibited the maturation process of the blood formation to form leaky blood vessels.

• Depletion of endothelial TGF-β signaling increase of circulated tumor cells, whereas pulmonary metastasis decreased compared to wild-type mice.

M219

Serum miRNAs associated with the presence and rapid expansion of abdominal aortic aneurysms

Vikram Iyer1,2,3,4, Thomas Watkins5, Erik Biros2, Smriti Krishna2, Joseph Moxon2, Susan Morton2, Sharon Lazzaroni2, Georgina Anderson2, Jenna Pinchbeck2, Lisan Yip2, John Miles5, John Bingley1, Jonathan Golledge1,2,3

1Faculty of Medicine, University of Queensland, Brisbane, Australia, 2Queensland Research Centre for Peripheral Vascular Disease, James Cook University, Townsville, Australia, 3Department of Vascular Surgery, The Townsville Hospital & Health Service, Douglas, Australia, 4Department of Vascular Surgery, The Royal Brisbane & Women’s Hospital, Herston, Australia, 5Australian Institute for Tropical Health & Medicine, James Cook University, Cairns, Australia

• Serum expression of let-7b-5p is associated with a diagnosis of abdominal aortic aneurysm in the tested cohort

• Serum expression of miR-1268a is negatively cor-related with rapid abdominal aortic aneurysm growth in the tested cohort

• The downstream targets and pathways associ-ated with let-7b-5p and miR-1268a may function-ally implicate these miRNAs in abdominal aortic aneurysm pathogenesis and progression

Posters – Tuesday

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IVBM2018

T001

Volume imaging of the rachis lymphatic net-work in rodents

PhD Laurent Jacob1, PhD Ligia Boisserand2, Julliette Pestel1, PhD Thomas Mathivet3, PhD Sandy Lee2, MD Eric Song4, MD-PhD Salli Antila5, Marie-Stéphane Aigrot1, PhD W Mark Saltzman6, PhD Nicolas Renier1, PhD Anne C Eichmann3,7, MD-PhD Kari Alitalo5, PhD Jean-Léon Thomas1,2

1Université Pierre et Marie Curie Paris 06 UMR S 1127, Sorbonne Université, Institut du Cerveau et de la Moelle Epinière, Paris, France, 2Departments of Neurology, Yale School of Medicine, New HAven, USA, 3INSERM U970, Paris Cardiovascular Research Center, 75015 Paris , France, 4Department of Immunobiology, Yale University, New Haven, USA, 5Wihuri Research Institute and Translational Cancer Biology Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland, 6Department of Biomedical Engineering, Yale University, New Haven, USA, 7Cardiovascular Research Center and the Department of Cellular and Molecular Physiology, 300 George Street, Yale University School of Medicine, New Haven, USA

• I-DISCO protocol combined with light sheet flu-orescence microscopy allows volume imaging of the spinal cord lymphatic system in adult mice.

• Spinal cord lymphatic vasculature closely inter-acts with leucocytes and the sympathetic ner-vous system.

• Spinal cord meningeal lymphatic vessels connect dorsally with subcutaneous tissues and ventrolat-erally with lymph nodes and lymphatic ducts.

T002

Role of medial vascular smooth muscle cells in atherogenesis and features of a vulnerable plaque

Armand Jaminon1, Brecht Willems1, Rick van Gorp1, Chiara Recarti1, Paul Schiffers1, Marc van Zandvoort1, Chris Reutelingsperger1, Murray Clarke2, Martin Bennett2, Leon Schurgers1

1Maastricht University, Maastricht, Netherlands, 2University of Cambridge, Cambridge, United Kingdom

• VSMC have important protective functions in ath-erosclerosis

• Medial VSMC ablation causes increased athero-sclerosis development and features of plaque instability

• The interplay between VSMC and endothelial cells seems to be crucial during atherosclerosis

T003

Axon guidance-related factor FLRT3 is a novel regulator of VEGF-signaling and endothelial cell function

Suvi Jauhiainen1,2, Johanna P. Laakkonen2, Pyry I. Toivanen2, Tiina Nieminen2, Anna-Liisa Levonen2, Seppo Ylä-Herttuala2,3

1Rudbeck Laboratory, University of Uppsala, Uppsala, Sweden, 2A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland, 3Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Fibronectin and leucine-rich transmembrane pro-tein-3 (FLRT3) is upregulated in human umbilical vein endothelial cells (HUVECs) by VEGFR-2 bind-ing ligands (VEGF-A, -D and -F).

• Experiments done with SU1498 confirm the importance of VEGFR-2 in the process

• Blockage of FLRT3 by siRNA techniques decreased HUVECs survival and in vitro angiogenesis, thus showing the importance of FLRT3 in HUVECs function.

T004

Loss of Angiopoietin-1/ Tie2 signaling in kid-ney disease aggravates capillary rarefaction and tubulointerstitial fibrosis

Susan E Quaggin1, Christer Betsholtz2,3, Marie Jeansson3

1Feinberg Cardiovascular Research Institute and Division of Nephrology and Hypertension, Chicago, USA, 2Integrated Cardio Metabolic Centre, Huddinge, Sweden, 3Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden

• Loss of endothelial Tie2 in experimental kidney disease decreases renal blood vessel perfusion and increases hypoxia

• Endothelial Tie2 deficiency in experimental kid-ney disease aggravates tubulointerstitial fibrosis

• Loss of endothelial Tie2 in experimental kidney disease increase colocalization of the endothelial lineage with aSMA, suggestive of increased endo-thelial-mesenchymal transition

Posters – Tuesday

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IVBM2018

T005

All you ever wanted to know about the pro-teolytic processing of vascular endothelial growth factor-C

Michael Jeltsch1,2

1University Of Helsinki, , Finland, 2Wihuri Research Institute, Helsinki, Finland

• Pro-VEGF-C cleavage by different proteases results in distinct forms of mature VEGF-C.

• Different anti-VEGF-C antibodies differ greatly in their ability to recognize different forms of VEGF-C.

• Any interpretation of VEGF-C data obtained with antibodies requires a validation of the antibody’s ability to recognize different VEGF-C forms.

T006

Endothelial Wnt/β-catenin signaling modu-lates mural cell numbers during retinal vascu-lar development

Nina Jensen1, Agnieszka Martowicz1, Marta Alabrudzinska1, Joanna Wisniewska-Kruk1, Monica Corada2, Elisabetta Dejana2, Daniel Nyqvist1

1Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden, 2IFOM - The FIRC Institute of Molecular Oncology, Milan, Italy

• Endothelial β-catenin gain-of-function increases mural cell coverage on veins in the postnatal mouse retina.

• In addition to immunohistochemical analysis of mural cell markers, we analyzed mural cell num-bers directly via a mural cell reporter mouse.

• We explore the mechanism via reporter mice and RNAscope In situ hybridization on whole mount retinas.

T007

Cell cycle control of lymph-venous sprouting

Ayelet Jerafi - Vider1, Karina Yaniv1


• Pre-specified venous and lymphatic ECs sprout from the CV at G0/G1 phases of the cell-cycle.

• p53 is specifically upregulated in CV ECs and con-trols lymph-venous sprouting

• Cell cycle arrest at G0/G1 results in precocious lympho-venous sprouting and defective lym-phatic differentiation.

T008

Strategy to enhance therapeutic efficiency of VEGF-C

Sawan Jha1, Khushbu Rauniyar1, Michael Jeltsch2, Kari Alitalo3

1Translational Cancer Biology Research Program, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland, 2Translational Cancer Biology Research Program, Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland, 3Translational Cancer Biology Research Program, Wihuri Research Institute, Biomedicum Helsinki, Helsinki University Central Hospital, University of Helsinki, Helsinki, Finland

• VEGF-C is a central therapeutic molecule in lymphangiogenesis.

• Combining VEGF-C together with its regulator as an approach to enhance lymphangiogenesis.

• Activation of lymphangiogenesis

T009

ACVR1/ALK2 Enables Venous Selective Pro-Angiogenic Responses to BMP Signaling

Suk-won Jin1

1Gwangju Institute Of Science And Technology, , South Korea

• BMP signaling selectively induces proliferation and sprouting angiogenesis from venous endo-thelial cells in mammals.

• Activin A Type I Receptor (ACVR1/ALK2) mediates the pro-angiogenic BMP signaling during angio-genesis.

T010

Src kinase family members c-Src, Yes and Fyn distinctly regulate vascular growth and func-tion

Yi Jin1, Lena Claesson-Welsh1

1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden

• Src family kinases, c-Src, Yes and Fyn show dis-tinct subcellular localization and different interac-tive partners.

• Yes, the most abundant SFK in endothelial cells, is localized at endothelial junctions while c-Src and Fyn are not.

• Yes appears in oscillating lamellipodia close to cell borders.

Posters – Tuesday

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IVBM2018

T011

Quantitative Analyses of Sprouting Angio-genesis in Developing Retinal Vasculature of Newborn Mice

Dong Hyun Jo1, Chang Sik Cho1, Seok Jae Lee1, Sang-Mok Lee2, Byung Joo Lee1, Jin Hyoung Kim1, Young Suk Yu3, Jeong Hun Kim1,3,4

1Fight against Angiogenesis-Related Blindness (FARB) Laboratory, Clinical Research Institute, Seoul National University Hospital, Seoul, South Korea, 2Department of Ophthalmology, Hallym University Sacred Heart Hospital, Gyeonggi-do, South Korea, 3Department of Ophthalmology, Seoul National University College of Medicine, Seoul, South Korea, 4Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, South Korea

• The sprouting retinal vasculature in newborn mice is the valuable tool to investigate organ-spe-cific dynamics and characteristics of tip cells.

• The number of tip cells peaked at postnatal day (P)6 and dramatically decreased from P6 to P8.

• The number of tip cells and vessel areas were sig-nificantly higher around veins compared to arter-ies.

T012

Peroxidasin is essential for endothelial cell behavior and signaling through contributing to extracellular matrix assembly

Young-Ae Joe1, Seung-Woo Lee1, Hyun-Kyung Kim1, Purevjargal Naidansuren1, Hong-Seok Choi1, Dong-Hoon Kang2, Sang-Won Kang2, Jeong-A Kim1

1Department of Meidical Lifescience and Cancer Research Institute, College of Medicine, The Catholic University of Korea, Seoul 06591, South Korea, 2Department of Life Sciences and Research Center for Cell Homeostasis, Ewha Womans University , Seoul 03760, South Korea

• Peroxidasin (PXDN) is required for endothelial cell behavior including proliferation, migration, and morphological differentiation, and for angiogenic process.

• PXDN functions extracellularly, and its unique role is evidenced by the necessity of both ECM motifs and peroxidase activity.

• PXDN is essential for fibrillar network assembly of collagen IV, fibronectin and laminin, and for full ECM-mediated signaling.

T013

Shear Stress and VE-Cadherin: The Molecular Mechanism of Vascular Fusion

Elizabeth Jones1, Hanna M. Peacock1, Bahar Kasaai1, Geertje Swennen2, Emma Gordon3, Lena Claesson-Welsh3, Peter Verhamme1, Elizabeth A.V. Jones1

1KU Leuven, Leuven, Belgium, 2Maastricht University, Maastricht, Netherlands, 3Uppsala University, Uppsala, Sweden

• Hyperfused plexus in embryos due to low shear stress and/or DAPT treatment occur due patho-logical levels of a process of vascular fusion.

• VE-Cadherin phosphorylation occurs during vas-cular fusion.

• Increasing shear stress can prevent fusion induced by DAPT by causing the association of VE-PTP and VE-Cadherin

T014

Key role for human bone marrow primary endothelial cells in the latest phase of mega-karyopoiesis

Camille Jost1,2,3,4, Nathalie Brouard1,2,3,4, Anita Eckly1,2,3,4, Henri De la Salle1,2,3,4, François Gastaud5, Christian Gachet1,2,3,4, François Lanza1,2,3,4

1Inserm UMR_S1255, Strasbourg, France, 2Etablissement Français du Sang, , France, 3Université de Strasbourg, , France, 4Fédération de Médecine Translationnelle, , France, 5Cabinet Gastaud, , France

• Prospective isolation and expansion of human bone marrow endothelial cells

• Human primary endothelial cells support the production of proplatelets from megakaryocyte progenitors more efficiently than primary human mesenchymal cells

• Human primary endothelial cells support pro-platelet production via a cell-cell contact depen-dent mechanism

Posters – Tuesday

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IVBM2018

T015

Sex differences in the lifestyle risk factors for ischemic heart disease among Koreans

JiAe Shin1, Dongwoo Ham2, Hyojee Joung1,2

1Department of Public Health, Graduate School of Public Health, Seoul National University, Seoul, South Korea, 2Institute of Health and Environment, Seoul National University, Seoul, South Korea

• Aimed to investigate associations between isch-emic heart disease and lifestyle risk factors according to sex using a nationwide cohort.

• Estimated the hazard ratios of lifestyle risk factors for ischemic heart disease using Cox proportional hazards multivariate regression models

• Found that men and women had different asso-ciations of meal types, alcohol consumption, and smoking with ischemic heart disease.

T016

The effects of Korean diet on the cardiovascu-lar risk factors: a randomized clinical trial

Seong-Ah Kim1,3, Young Hwang2, Young-Hee Park2, Min-Sook Kang2, Hyojee Joung1,3

1Graduate School of Public Health, Seoul National University, Seoul, South Korea, 2Department of Agro-food Resources, National Institute of Agricultural Sciences, Rural Development Administration, Wanju, South Korea, 3Institute of Health and Environment, Seoul National University, Seoul, South Korea

• This study was performed to assess the effects of Korean diet (KD) on cardiovascular risk factors compared with typical American diet (TAD) and healthy American diet (HAD).

• The study design was a randomized crossover clinical trial, that 54 subjects consumed each diet for four-week.

• The KD reduced total cholesterol, LDL cholesterol, and triglycerides among Korean adults.

T017

Dual antiplatelet and anticoagulant APAC attenuates procoagulant activity and targets vascular injury site without bleeds

Annukka Jouppila1, Karina Barreiro2, Riikka Tulamo3, Anders Albäck3, Riitta Lassila4,5

1HUCH Research Institute, Helsinki, Finland, 2Institute for Molecular Medicine Finland FIMM, University of Helsinki, Helsinki, Finland, 3Department of Vascular Surgery, Helsinki University Hospital and University of Helsinki, Helsinki, Finland, 4Coagulation Disorders Unit, University of Helsinki and Departments of Hematology and Clinical Chemistry (HUSLAB Laboratory Services), Comprehensive Cancer Center, Helsinki University Hospital, Helsinki Finland, Helsinki, Finland, 5Aplagon Oy, Helsinki, Finland

• APAC is a semisynthetic mimetic of mast cell-de-rived heparin proteoglycans, developed for anti-thrombotic management during vascular inter-ventions and inhibiting reperfusion injury

• APAC is a dual inhibitor of collagen- and throm-bin-induced platelet aggregation and blood coag-ulation, but maintains platelet activity via other routes

• APAC rapidly targets injured subendothelial ves-sel co-localizing with matrix von Willebrand fac-tor and laminin

T018

The anticoagulant vitamin k-dependent factor, protein S, regulates vascular permeability

Aurélie Joussaume1,2, Chryso Kanthou3, Fatima Dkhissi1, Omar Benzakour1

1Inserm U1082, Poitiers, France, 2CHU de Poitiers, Poitiers, France, 3Cancer Research UK Tumour Microcirculation Group, Department of Oncology and Metabolism, School of Medicine and Biomedical Sciences, Sheffield, United Kingdom

• ProS increases the permeability of endothelial cell monolayers and enhances VEGF-A-induced endothelial cell permeability.

• ProS activates P38/HSP27 pathway and induces the phosphorylation of VE-cadherin.

• ProS may be a novel endogenous regulatory mechanism for the endothelium.

Posters – Tuesday

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IVBM2018

T019

PLODs and LOX participate in vascular smooth muscle cell calcification

Eva Jover1,2, Ana Silvente1, Francisco Marín1,3, José Martínez-González3,4, Mar Orriols3, Carlos M. Martinez5, Carmen María Puche1, Mariano Valdés1,3, Cristina Rodriguez3,6, Diana Hernández-Romero1,3

1Hospital Clínico Universitario Virgen de la Arrixaca, Universidad de Murcia, IMIB-Arrixaca, El Palmar, Spain, 2University of Bristol, Bristol, United Kingdom, 3CIBER de Enfermedades Cardiovasculares (CIBERCV), , Spain, 4Instituto de Investigaciones Biomédicas de Barcelona (IIBB-CSIC), IIB-Sant Pau, Barcelona, Spain, 5CIBER de Enfermedades Hepáticas y Digestivas (CIBERehd), Spain, 6Institut de Recerca del Hospital de la Santa Creu i Sant Pau-Programa ICCC, IIB-Sant Pau., Barcelona, Spain

• Enzymes involved in collagen cross-linking and maturation, such as LOX and PLOD, are induced in calcifying vascular smooth muscle cells

• In vitro and ex vivo vascular mineralization and osteoblast transdifferentiation are associated with the amount of mature collagen and that may have a clinical impact

• LOX and PLOD emerge as new players in vascular calcification

T020

Cardiac microvascular endothelial cells improve cardiomyocyte function: the role of nitric oxide and empagliflozin treatment

Rio Juni1,2, Diederik Kuster1,2, Max Goebel1,2, Jolanda van der Velden1,2, René Musters1,2, Pieter Koolwijk1,2, Walter Paulus1,2, Victor van Hinsbergh1,2

1VU University Medical Center, Amsterdam,, The Netherlands, 2Amsterdam Cardiovascular Sciences, Amsterdam,, The Netherlands

• Cardiac microvascular endothelial cells (CMEC) directly regulate cardiomyocyte (CM) systolic and diastolic function.

• Nitric oxide is required for the beneficial effect of CMEC on CM contractility.

• The positive effect of CMEC on CM contractile profiles is impaired by TNF-α and can be restored by empagliflozin.

T021

Increasing Biointegration of Small Diameter Vascular Grafts by Reactive Ion Plasma Mod-ification

Patrick Jurney1, Deirdre Anderson1, Grace Pohan2, Evelyn Yim2, Monica Hinds1

1Oregon Health & Science University, Portland, United States, 2University of Waterloo, Waterloo, Canada

• Poly(vinyl-alcohol) is a bio-compatible polymer with desirable material properties for small diam-eter vascular grafts but is chemically inert.

• Reactive ion plasma introduces surface reac-tive groups and nanotopography to PVA which increases EC affinity and does not increase thrombogenicity.

• Surface chemistry and topography can be altered through the carrier gas, power, and treatment time of reactive ion plasma.

T022

Monitoring intra-arterial mannitol based blood brain barrier opening with novel non-invasing sensing techniques

Mika Kaakinen1, Teemu Myllylä2,3, Jari Jukkola1, Aleksandra Zienkiewicz3, Erkki Vihriälä3, Vesa Korhonen2,4, Vesa Kiviniemi2,4, Lauri Eklund1

1Biocenter Oulu, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland, 2 Research Unit of Medical Imaging, Physics and Technology, University of Oulu. , Oulu, Finland, 3Optoelectronics and Measurement Techniques Unit, University of Oulu , Oulu, Finland, 4Department of Diagnostic Radiology, Oulu University Hospital, Oulu, Finland

• BBB can be opened efficiently in laboratory mice by using intra arterial mannitol injection.

• Non-invasive monitoring techniques are prom-ising for assessing safety and efficiency of BBB opening.

• Non-invasive monitoring techniques can be used in both mice and humans.

Posters – Tuesday

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IVBM2018

T023

Disease modelling in a dish –induced pluripo-tent stem cells-derived endothelial cells from HNF1A-MODY patients

Neli Kachamakova-Trojanowska1, Jacek Stepniewski2, Kalina Andrysiak2, Alicja Jozkowicz2, Jozef Dulak2,3

1Malopolska Centrum of Biotechnology, Jagiellonian University, Krakow, Poland, 2Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland, 3Kardio-Med Silesia, Zabrze, Poland

• Two tested differentiation protocols, for obtaining endothelial cells from control and HNF1A-MODY hiPSCs, show major difference in the efficiency.

• Purified and cultured hiPS-EC, generated with both protocols, differed in the expression of CD31, VE-cadherin and VEGFR2.

• hiPS-EC, from both protocols and from all cell lines tested, show similar phospho-eNOS expres-sion and angiogenic capacity.

T024

Developmentally regulated chromatin interac-tions orchestrate transcriptional changes in endothelial cells during vasculogenesis and angiogenesis

Henri Niskanen1, Irina Tuszynska2, Rafal Zaborowski2, Maria Bouvy-Liivrand3, Ana Hernández de Sande3, Merja Heinäniemi3, Seppo Ylä-Herttuala1,4, Bartek Wilczynski2, Minna Kaikkonen1

1A.I.Virtanen Institute, University Of Eastern Finland, Kuopio, Finland, 2Institute of Informatics, University of Warsaw, Warsaw, Poland, 3School of Medicine, University of Eastern Finland, Kuopio, Finland, 4Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Endothelial cell differentiation is encompassed by extensive switching between chromatin com-partment states and establishment of long-range interactions involving heterochromatin.,

• Transcriptional changes in response to pro-an-giogenic stimuli occur at developmentally pre-es-tablished chromatin compartments characterized by high chromatin accessibility and super-en-hancers.,

• Chromatin interactions within topologically asso-ciated domains provide insight into the regu-latory environment of key identity genes and pri-miRNAs.

T025

Vasculogenesis of mouse embryonic kidneys and organoids in a chicken chorioallantoic membrane (CAM) culture approach

Susanna Kaisto1, Ilya Skovorodkin1, Ilkka Miinalainen2, Seppo Vainio1

1University of Oulu, , Finland, 2Biocenter Oulu, , Finland

• Endothelial cells of mouse kidneys and kid-ney organoids transplanted to chicken embryo revealed to be of donor origin.

• Glomerular vasculature develops in mouse kid-neys and renal organoids transplanted to chicken embryo, while in organotypic kidney cultures glomeruli remain avascular.

• Chicken CAM- and intracoelomic xenotransplan-tation offers ways to vascularize organoids ex vivo

T027

Integrative analysis of lymphedema-induced adipose tissue

Sinem Karaman1, Riikka Kivela1, Cheng Zhang2, Satu Lehti1, Alexander Kanitz3, Marja-Riitta Taskinen4, Håkan Brorson5,6, Adil Mardinoglu2, Kari Alitalo1

1Wihuri Research Institute and University Of Helsinki, Helsinki, Finland, 2Science for Life Laboratory, KTH-Royal Institute of Technology, Stockholm, Sweden, 3Biozentrum, University of Basel and Swiss Institute of Bioinformatics, Basel, Switzerland, 4Heart and Lung Center, Helsinki University Hospital, Finland and Diabetes and Obesity Program, University of Helsinki, Helsinki, Finland, 5Department of Clinical Sciences in Malmo, Lund University, Malmo, Sweden, 6Department of Plastic and Reconstructive Surgery, Skane University Hospital, Malmo, Sweden

• Lymphedema induces-adipose tissue accumula-tion

• The results suggest changes in nucleotide and amino acid metabolism

• Evidence of increased alternative splicing events affecting components of the ribosome

Posters – Tuesday

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IVBM2018

T028

Functional Studies on the EPHB4 Signalling Pathway in Patients with Generalised Lym-phatic Dysplasia

Christina Karapouliou1, Silvia Martin-Almedina1, Steve Jeffery1, Pia Ostergaard1

1Molecular & Clinical Sciences Institute, St George’s University of London, London, United Kingdom

• EPHB4-kinase inactivating mutations are associ-ated with Generalized Lymphatic Dysplasia and the receptor was identified as critical regulator of lymphangiogenesis.

• This study aims to functionally characterize the specific mutations and further investigate the role of EPHB4 in lymphangiogenesis.

• EPHB4 mutations may reduce MAPK signalling. EPHB4 depletion/inhibition impairs cytoskeleton organisation, migration and tube formation in Lymphatic Endothelial Cells.

T029

Chymase released from hypoxia-activated cardiac mast cells cleaves human apolipopro-teinA-I and compromises its cardioprotective activity

Ilona Kareinen1,2, Marc Baumann3, Su Duy Nguyen1, Katariina Maaninka1, Andrey Anisimov1,4, Minoru Tozuka5, Matti Jauhiainen6, Miriam Lee-Rueckert1, Petri Kovanen1

1Wihuri Research Institute, Helsinki, Finland, 2Department of Veterinary Biosciences, Faculty of Veterinary Medicine, University of Helsinki, and Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Helsinki / Stockholm, Finland / Sweden, 3Protein Chemistry Unit, Institute of Biomedicine/Anatomy, University of Helsinki, Helsinki, Finland, 4Translational Cancer Biology Program, University of Helsinki, Helsinki, Finland, 5Analytical Laboratory Chemistry, Graduate School of Health Care Sciences, Tokyo Medical and Dental University, Tokyo, Japan, 6Minerva Foundation Institute for Medical Research, and National Institute for Health and Welfare , Helsinki, Finland

• Mast cell activation in rat heart Langendorff per-fusion system results in chymase-dependent cleavage of human apolipoprotein A-I at Tyr192

• The common proteolytic end-product of apoA-I generated by the action of human or rat chymase is the Tyr192-truncated fragment

• Lipid-free apoA-I and reconstituted-HDL (rHDL) particles promote migration of cultured endo-thelial cells, but lose this capacity after chy-mase-treatment

T030

Critical role of tumor lymphatic function in regulating tumor inflammatory and immuno-suppressive microenvironment

Raghu Kataru1, Babak Mehrara1

1Memorial Sloan Kettering Cancer Center, New York, United States

• Peri-tumoral stroma is filled with edematous fluid and is increased in lymphatic ablated tumors.

• Lymphatic ablation causes enhanced tumor growth, exacerbated peri-tumor edema, enhanced inflammation, immunosuppression compared to controls.

• Lymphatic ablation causes reduced CTL infiltra-tion into tumor foci with increased PD-L1 expres-sion compared to controls.

T031

Osteogenic environment accompanies brain capillary calcification in the mouse model of primary familial brain calcification

Yvette Zarb1, Ulrike Weber-Stadlbauer2, Daniel Kirschenbaum3, Diana Kindler4, Jan Klohs4, Adriano Aguzzi3, Annika Keller1

1Dept. of Neurosurgery, Zurich University Hospital/Zurich University, Zurich, Switzerland, 2Inst. of Pharmacology and Toxicology, University of Zurich-Vetsuisse, Zurich, Switzerland, 3Inst. of Neuropathology, Zurich University Hospital/Zurich University, Zurich, Switzerland, 4Institute for Biomedical Engineering, ETH, Zurich, Switzerland

• Vessel-associated calcifications in Pdgfb ret/ret animals express markers for osteoblasts, osteo-clasts and osteocytes.

• There is a high inter-individual variation in calcifi-cation load in Pdgfb ret/ret animals.

• Pdgfb ret/ret animals show behavioral features such as increased anxiety and reduced pre-pulse inhibition, which recapitulate neuropsychiatric symptoms described in PFBC patients

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IVBM2018

T032

Perivascular cell-specific knockout of plu-ripotency gene Oct4 inhibits angiogenesis by attenuating perivascular and endothelial migration

Molly Kelly-Goss1,2, Daniel Hess1,3, Olga Cherepanova1,4, Anh Nguyen1, Brian Annex1,5, Shayn Peirce1,2, Gary Owens1,4

1Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, United States, 2Department of Biomedical Engineering, University of Virginia, Charlottesville, United States, 3Department of Biochemistry and Molecular Genetics, University of Virginia, Charlottesville, United States, 4Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, United States, 5Department of Medicine, Cardiovascular Medicine, University of Virginia, Charlottesville, United States

• Stem cell pluripotency gene Oct4 knockout in smooth muscle cells and pericytes (SMC-P) leads to aberrant, leaky angiogenesis in response to corneal alkali-burn and hindlimb ischemia.

• SMC-P Oct4 knockout leads to impaired SMC-P investment, SMC-P migration, and endothelial migration.

• SMC-P Oct4 knockout leads to dysregulated Slit3/Slit2 expression. SLIT3/SLIT2 leads to aberrant SMC-P and endothelial migration in vitro.

T033

Chr4D70kb/D70kb x LDLR-/-/ApoB100/100, a new mouse model for atherosclerosis?

Sanna Kettunen1, Seppo Ylä-Herttuala1

1 University of Eastern Finland, Kuopio, Finland

• A knockout mouse model for human Chr9p21 risk interval may help to reveal mechanisms behind the genetic atherosclerosis risk

• “ANRIL KO” mice in LDLR-/- ApoB100/100 back-ground show increased atherosclerosis compared to the controls

• The risk interval associated differences in athero-sclerosis appear to be independent of other risk factors

T034

Novel small molecule ERK inhibitor identified by high-throughput-compound-screening that suppresses angiogenesis, retinal permeability and arthritis

Levon Khachigian1, Yue Li1, Mei-Chun Yeh1,2, Ahmad Alhendi1, Mina Elahy1

1Vascular Biology and Translational Research, University of New South Wales, Sydney, Australia, 2Queensland University of Technology, Brisbane, Australia

• We identified BT2 from a library of >100K com-pounds. BT2, which hitherto has no known func-tion, blocks angiogenesis in mice.

• BT2 is a potent inhibitor of ERK1/2 phosphoryla-tion. BT2 suppresses retinal permeability in both rabbits and rats, and arthritis in mice.

• Intraperitoneal, intraarticular or gavage adminis-tration of BT2 in mice produced no histopatho-logical evidence of toxicity.

T035

Lymphangiogenesis is increased in aortitis and may reveal susceptibility for dissection

Ivana Kholova1,2, Eetu Niinimäki4, Ari Mennander3, Timo Paavonen1,2

1University Of Tampere, Tampere, Finland, 2Fimlab Laboratories, Tampere, Finland, 3Heart Hospital, Tampere, Finland, 4South Carelian Hospital, Lappeenranta, Finland

• Lymphangiogenesis was studied in normal and diseased human aortas. Lymphatics were local-ized in the adventitia and periadventitial tissue.

• The mean lymphatic density was 10.1+/-3.8 in aortitis vs 5.9+/-4.2 in controls( p = 0.023).

• IAL is increased in aortitis as compared with aor-tas without inflammation.

T036

Identification of Sfrp1 as a novel angiocrine factor for cancer stem cell maintenance

Hiroyasu Kidoya1, Yumiko Hayashi1, Fumitaka Muramatsu1, Nobuyuki Takakura1

1Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Japan

• Tumor growth was significantly suppressed in Sfrp1 deficient mice.

• SFRP1 was locally produced from tumor endothe-lium.

• Cancer stem cells were reduced in tumor tissue of Sfrp1 deficient mice.

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IVBM2018

T037

Crosstalk of VEGFs, BMPs and Hippo signal-ing pathway in angiogenesis

Miika Kiema1, Heidi Pulkkinen1, Jari Lappalainen1, Mustafa Beter1, Henna Ilmonen1, Annakaisa Tirronen1, Lari Holappa1, Henri Niskanen1, Minna Kaikkonen1, Seppo Ylä-Herttuala1,2,3, Johanna Laakkonen1

1A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, 2Science Service Center, Kuopio University Hospital, Kuopio, Finland, 3Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Transcriptional programming of VEGF-mediated angiogenesis is only partially understood, and the knowledge is needed for development of angio-genic therapies.

• VEGF upregulates expression of multiple growth factors in vivo, including bone morphogenetic proteins that modulate endothelial cell sprouting and elongation.

• Hippo pathway, known for VEGFR2 recycling, have pleiotropic effects on cells by regulating sig-naling of multiple factors involved in angiogene-sis.

T038

Angiopoietin-2 variant affects mammary gland tumor growth and lung metastasis

Minna Kihlström1, Riikka Pietilä1, Emmi Kapiainen1, Anna Laitakari1, Mika Kaakinen1, Harri Elamaa1, Lauri Eklund1

1Oulu Centre for Cell-Matrix Research, Faculty of Biochemistry and Molecular Medicine, Biocenter Oulu, University of Oulu, Oulu, Finland

• N-terminal domain of Ang2 is not necessary for physiological angiogenesis in mouse retina model

• Growth of mammary gland tumors is delayed in double-transgenic PyMT; Ang2+/443 mice

• Ang2-443 protein form is potent to enhance tumor cell endothelial transmigration and lung metastasis of B16F10 melanoma cells

T039

RANKL blockade suppresses pathological angiogenesis and vascular leakage in an oxy-gen-induced retinopathy model

Jaetaek Kim1, Sangmi Ock1, Junyeop Lee2, Joong -Yeol Park3

1Department of Internal Medicine, College of Medicine, Chung-Ang University, Seoul, South Korea, 2Department of Ophthalmology, College of Medicine, Yeungnam University, Daegu, South Korea, 3Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

• RANKL • retina pathological angiogenesis • vascular leakage

T040

Endothelial pyruvate kinase M2 maintains vascular integrity

Boa Kim1, Cholsoon Jang2, Harita Dharaneeswaran1, Jian Li1, Mohit Bhide1, Steven Yang1, Zolt Arany1

1University Of Pennsylvania, Philadelphia, United States, 2Princeton University, Princeton, United States

• Endothelial cells express PKM2 almost exclusively over PKM1.

• In proliferating endothelial cells, PKM2 is required to suppress p53 and maintain cell cycle progres-sion.

• In quiescent endothelial cells, PKM2 is required to maintain tight barrier function.

T041

The pathological effect of alpha-Synuclein on the brain vascular structure and integrity

Do-geun Kim1, Jin-Young Jeong1, Mal-Gi Choi1, Mi Jin Kim1, Ri Yu1, Won-Jong Oh1

1Korea Brain Research Institute, Daegu, South Korea

• Peripherally injected abnormal α-Syn induces acute brain vasculopathy.

• Animal model of PD shows abnormal brain vascu-lar structure with blood brain barrier breakdown.

• Significant interaction of α-Syn with multiple plasma factors induces the vasculopathy.

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IVBM2018

T042

Oncolytic vaccinia virus mpJX-594 targets tumor vasculature and synergizes with anti-PD-1 immune checkpoint inhibitor

Minah Kim1, Aishwarya Subramanian1, Howard Cha1, Maximilian Nitschké1, Barbara Sennino1, Jun Gu Bae2, Jiwon Choi2, Naomi Silva3, Donald McDonald1

1University Of California San Francisco, San Francisco, United States, 2SillaJen Biotherapeutics Inc, Seoul, South Korea, 3SillaJen Biotherapeutics Inc, San Fancisco, United States

• mpJX-594, oncolytic vaccinia virus induces rapid infection of tumor vascular endothelial cells and subsequent infection of tumor cells in RIP-Tag2 transgenic mice

• mpJX-594 and anti-PD-1 antibody have stron-ger antitumor actions when given together than either agent has alone.

• mpJX-594 and anti-PD-1 antibody results in increase of CD8 T-cell infiltration and vascular specialization expressing MECA79.

T043

SALM4 Regulates Angiogenic Functions Through VEGFR2 phosphorylation.

Dong Young Kim1, Eunkyung Lie2, Mr. Eunjoon Kim2, Young-Guen Kwon1

1Yonsei University, Seodaemun-gu, South Korea, 2Korea Advanced Institute for Science and Technology, Yusung-gu, South Korea

• SALM4 expression was increased during differen-tiation from Endothelial progenitor cells to Endo-thelial cells (ECs).

• Inhibition of SALM4 reduced EC migration, tube formation, survival and sprouting.

• SALM4 regulates VEGFR2 activation and its down-stream signaling.

T044

Myocardial angiopoietin-1 is indispensable for atrial chamber morphogenesis

Kyun Hoo Kim1,5, Myungjin Yang1,5, Yoshikazu Nakaoka2,3, Hellmut Augustin4, Gou Young Koh1,5

1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, South Korea, 2Department of Vascular Physiology, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan, 3Department of Cardiovascular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan, 4Division of Vascular Oncology and Metastasis, German Cancer Research Center Heidelberg, Heidelberg, Germany, 5Center for Vascular Research, Institute for Basic Science, Daejeon, South Korea

• Loss of myocardial Angpt1 impairs atrial chamber morphogenesis of mouse embryo.

• Myocardial Angpt1/endocardial Tie2 signaling promotes ADAMTS-mediated degradation of car-diac jelly.

• Spatiotemporal degradation of cardiac jelly in atrium is crucial for regulation of myocardial pro-liferation and chamber maturation.

T045

Development of Venous Malformation Animal Model Using CRISPR-Cas9 Genome Editing of Tie2 L914F

Seo Ki Kim1, Sukhyun Song2, Mei-Yu Qiu1, Dongkyu Kim2, Gou Young Koh1,2

1Graduate School Of Medical Science And Engineering, Korea Advanced Institute Of Science And Technology, Daejeon, South Korea, 2Center for Vascular Research, Institute for Basic Science, Daejeon, South Korea

• Using CRISPR-Cas9, we established a human embryonic stem cell line containing homozygous single nucleotide mutation of L914F in Tie2.

• L914F ECs exhibited resistance to inhibitors tar-geting receptor tyrosine kinase (RTK)-PI3K-AKT axis.

• BRD4 inhibitors and direct RTK inhibitors might be novel rescue strategies to overcome drug resistance in L914F ECs.

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IVBM2018

T046

Laminar flow inhibits ER stress-induced endo-thelial apoptosis through PI3K/Akt-dependent signaling pathway

Suji Kim1, Jung-Hwa Han1, Sujin Kim1

1Yeungnam University, Gyeongsangbuk-do/Daegu, South Korea

• atherosclerosis• Laminar flow• ER stress

T047

Quercetin-induced apoptosis ameliorates vas-cular smooth muscle cell senescence through AMP-activated protein kinase signaling path-way

Seul Gi Kim1, Jin Young Sung1, Hyoung Chul Choi1

1Yeungnam University, Daegu, South Korea

• During the progression of ceullular senescence, cell have a resistnace to apoptosis.

• Quercetin-activated AMPK signaling pathway is ameliorates oxidative stress-induced senescence by increasing apoptosis.

T048

Modified the evans blue dye (EBD) dosage with NIR image to realize BBB breakdown

Hyung-seok Kim1, Hye-Won Ryu1, Jong-Tae Park1, Assistant Hoon Hyun3, Associated Man-Seok Park2, Assistant Kang Ho Choi2

1Department of Forensic medicine, Chonnam National University Medical School, Gwangju, South Korea, 2Department of Neurology, Chonnam National University Medical School, Gwangju, South Korea, 3Department of Biomedical Sciences, Chonnam National University Medical School, Gwangju, South Korea

• NIR fluorescence-assisted method is sensitive, simple, and could potentially provide new oppor-tunities to study BBB leakage

• Using small amount of EBD in different pathologi-cal conditions is available

• This method gives a chance to reduce the turnaround time and is a great advantage to researcher to get appropriate results.

T049

The Associations of Epicardial Adipose Tissue with Coronary Artery Disease and Coronary Atherosclerosis

Se-Hong Kim1, Ju-Hye Chung1

1Catholic University Of Korea, Seoul, South Korea

• Epicardial adipose tissue (EAT) volume measured by CT is associated with the severity of coronary artery disease (CAD).

• EAT were significantly associated with the pres-ence of CAD and coronary artery plaque burden.

• EAT may give important information for risk eval-uation in CAD.

T050

Hic-5 regulates the tumorigenesis of colorec-tal cancer through stromal remodeling.

Joo-ri Kim-kaneyama1, Tomokatsu Omoto1, Xiao-Feng Lei1, Aya Miyauchi1, Lin Gao1, Shogo Haraguchi1, Takuro Miyazaki1, Akira Miyazaki1

1Showa Univ., Tokyo, Japan

• Hic-5 is a focal adhesion protein involved in mechanotransduction.

• Stromal Hic-5 regulates lysyl oxidase expression and cancer cell proliferation.

• Hic-5 in carcinoma-associated fibroblasts regu-lates the development of colorectal carcinoma via the control of its microenvironment.

T051

Ultrafast MREG imaging of human glymphatic cardiovascular pulse trajectories.

M.Sc Zalan Rajna1, MD Heli Mattila1, BSc Lauri Raitamaa1, Tapio Seppänen1, Vesa Kiviniemi2

1Center for Machine Vision and Signal Analysis, University of Oulu, Oulu, Finland, 2Oulu Functional NeuroImaging, University of Oulu, Oulu, Finland

• Human glymphatic pulse trajectories can be imaged non-invasively

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IVBM2018

T052

IGF2 and IGF1R identified as novel tip cell genes in primary microvascular endothelial cell monolayers

Ingeborg Klaassen1, Marchien Dallinga1, Bahar Yetkin-Arik1, Ilse Vogels1, Ron Van Noorden1, Reinier Schlingemann1, Patrycja Nowak-Sliwinska3, Arjan Griffioen1

1Ocular Angiogenesis Group, Department of Ophthalmology and Department of Medical Biology, Academic Medical Center at the University of Amsterdam, Amsterdam, The Netherlands, 2Angiogenesis Laboratory, Department of Medical Oncology, VU University Medical Center, Amsterdam, The Netherlands, 3School of Pharmaceutical Sciences, University of Geneva, Geneva, Switzerland

• Tip cells, sprouting angiogenesis, CD34

T053

Optoacoustic imaging of hemodynamic dys-function and protease activity in a mouse model of ischemic stroke

Ruiqing Ni1, Markus Vaas1, Wuwei Ren1, Jan Klohs1

1University Of Zurich And ETH Zurich, Zurich, Switzerland

• Non-invasive optoacoustic imaging enables simultaneous visualization of vascular pathology in an experimental mouse model of ischemic stroke with high resolution

• Label-free multi-spectral optoaocustic imaging reveals disturbed hemodynamic function

• A protease-activatable optoacoustic sensor reports protease activity in the ischemic territory in vivo

T054

Inhibition of microRNA-146a enhances angio-genesis and functional recovery after myocar-dial infarction and hindlimb ischemia

Kai Knoepp1, Laura Korte1, Jochen Dutzmann1, Jan-Marcus Daniel1, Johann Bauersachs1, Daniel Sedding1

1Dept. of Cardiology, Hannover Medical School, Hannover, Germany

• Micro-RNA-146a is strongly upregulated in endo-thelial cells under ischemic conditions in vitro and in vivo.

• Blocking miR-146a enhances the regenerative capacitiy of EC, as well as angiogenesis and vas-cular regeneration in vivo.

• Blocking miR-146a preserves/restores cardiac function following myocardial infarction.

T055

A Novel Injection-Molded Microfluidic Plat-form with Radial Chemotactic Gradient

Jihoon Ko1, Younggyun Lee1, Somin Lee1, Byungjun Lee1,2, Noo Li Jeon1,2

1Seoul National University, Seoul, South Korea, 2Curiochips inc., Seoul, South Korea

• Injection-molded microfluidic platform• Angiogenesis assay• Vasculogenesis assay

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IVBM2018

T056

Hepatic angiocrine signaling guides metabolic homeostasis through balancing systemic iron levels and controlling liver size

Philipp-Sebastian Koch1,2, Thomas Leibing1,2, Victor Olsavszky1,2, Friederike Ulbrich1, Iris Augustin3,4, Michael Boutros3, Hellmut G. Augustin2,5,6, Jürgen G. Okun7, Claus-Dieter Langhans7, Carsten Sticht8, Alexandra Demory1, Sebastian A. Wohlfeil1,2, Thomas Henzler9, Mathias Meyer9, Johanna Zierow1,2, Sven Schneider10, Katja Breitkopf-Heinlein11, Haristi Gaitantzi11, Bradley Spencer-Dene12, Bernd Arnold13, Kay Klapproth14, Kai Schledzewski1,2, Cyrill Géraud1,2, Sergij Goerdt1,2

1Department Of Dermatology, Venereology And Allergology, Medical Faculty Mannheim, Heidelberg University, Germany Mannheim, Germany, 2European Center for Angioscience, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, Mannheim, Germany, 3German Cancer Research Center (DKFZ), Division of Signaling and Functional Genomics and Heidelberg University, Faculty of Medicine Mannheim, Department of Cell and Molecular Biology, Heidelberg, Germany, Heidelberg, Germany, 4Molecular Cell Biology and Plant Cell Technology, University of Applied Sciences Weihenstephan-Triesdorf, Freising, Germany, Freising, Germany, 5Division of Vascular Oncology and Metastasis (DKFZ-ZMBH Alliance), DKFZ, Heidelberg, Germany, Heidelberg, Germany, 6Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, Mannheim, Germany, 7Department of General Pediatrics, Division of Inherited Metabolic Diseases, University Children’s Hospital, Heidelberg, Germany, Heidelberg, Germany, 8Center for Medical Research, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, Mannheim, Germany, 9Institute of Clinical Radiology and Nuclear Medicine, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, Mannheim, Germany, 10Institute for Clinical Chemistry, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, Mannheim, Germany, 11Section of Molecular Hepatology, Second Medical Department, University Medical Center and Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, Mannheim, Germany, 12Experimental Histopathology Laboratory, The Francis Crick Institute, London, United Kingdom, London, UK, 13Division of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany, Heidelberg, Germany, 14Division of Cellular Immunology, German Cancer Research Center, Heidelberg, Germany, Heidelberg, Germany

• Organ-specific microvascular endothelial cells control the tissue microenvironment by endothe-lial-derived angiocrine factors

• Angiocrine Bmp2 signaling in the liver controls iron homeostasis

• Angiocrine Wnt signaling controls liver growth and metabolic maturation

T057

Brain photothrombotic injury induces VEGF-dependent pathologic angiogenesis and sustained vascular leakage

Bong-Ihn Koh1, Ju-Hee Kim1, Yoshiaki Kubota2, Injune Kim1

1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea, 2Department of Anatomy, Keio University School of Medicine, Tokyo, Japan

• Brain photothrombotic injury induces active angiogenesis preferentially in the pia mater ves-sels compared to cerebral cortex vessels

• Recovered vessels lack brain vessel-specific matu-rity and proper perivascular coverage by peri-cytes and astrocytes, contributing to sustained vascular leakage

• Injury-induced angiogenesis is driven by active VEGF-VEGFR2 signaling, which can be blocked to inhibit sustained vascular leakage

T058

Lower hemoglobin levels associate with lower body mass index and healthier metabolic pro-file

Peppi Koivunen1

1University Of Oulu, Finland

• Normal variation in hemoglobin levels was used as a measure to detect tissue oxygenation status

• Systemic activation of the hypoxia response by lower hemoglobin levels associated with protec-tion against obesity and metabolic dysfunction

• Metabolic syndrome is a potential new indication for HIF prolyl hydroxylase inhibitors

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IVBM2018

T059

A novel mouse model expressing human VEGF-A165 to age-related macular degener-ation

Emmi Kokki1, Tommi Karttunen2, Mrs. Venla Olsson1, Kati Kinnunen2,3, Seppo Ylä-Herttuala1,4

1A.I. Virtanen Institute, University Of Eastern Finland, Kuopio, Finland, 2Department of Ophthalmology, Kuopio University Hospital, Kuopio, Finland, 3Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland, 4Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• The aim was to develop a novel mouse model of age-related macular degeneration by induc-ing human VEGF-A165 expression by subretinal adenoviral Cre gene transfer into loxP-STOP-hVEGF-A165 transgenic mouse eye.

• After 2 weeks hVEGF-A165 led to subretinal neo-vascular membrane, increased retinal thickness and hyperfluorescense.

• Within 12 weeks neovascularization decreased being replaced by subretinal fibrosis and dru-sen-like deposits.

T060

Lineage specific requirement for RNA and DNA unwinding during lymphatic endothelial cell proliferation

Kaska Koltowska1,2, Kazuhide Shaun Okuda2, Maria Rondon Galeano2, Scott Paterson2, Anne Karine Lagendijk2, Jun Chen2, Gregory Baillie2, Ignaty Leshchiner3, Wolfram Goessling3, Kelly Smith2, Cas Simons2, Stefan Schulte-Merker4, Ben Hogan2

1Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 2Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia, 3Brigham and Women’s Hospital, Harvard Stem Cell Institute, Boston, USA, 4Institute of Cardiovascular Organogenesis and Regeneration, WWU Münster, Münster, Germany

• Unexpected lymphatic role for RNA and DNA unwinding enzymes during the lymphatic devel-opment.

• Ddx21 and top3a are necessary downstream components of vegfc/vegfr3 signalling pathway.

• Cell type specific regulation of proliferation during vascular development

T061

ORP2 controls endothelial cell polarization and angiogenic tube formation in vitro

Annika Koponen1, Annukka KIvelä1, Henriikka Kentala1, Amita Arora1, Vesa Olkkonen1,2

1Minerva Foundation Institute For Medical Research, Helsinki, Finland, 2Department of Anatomy, Faculty of Medicine, University of Helsinki, Helsinki, Finland

• ORP2 belongs to the family of OSBP-related pro-teins mediating lipid transport and signaling at intracellular membrane contact sites.

• ORP2 localizes in HUVECs at lipid droplet-ER con-tacts, endosomes and sites of dynamic F-actin polymerisation underneath the plasma mem-brane.

• ORP2 overexpression induces polarised cell sur-face protrusions and its knock-down results in an inhibition of angiogenic tube formation in vitro.

T062

NFAT5/TonEBP - a mechanosensitive tran-scription factor in vascular smooth muscle cells controlling arterial remodeling

Maren Zappe1, Anja Feldner1, Caroline Arnold1, Markus Hecker1, Wolfgang Neuhofer2, Thomas Korff1

1Institute of Physiology and Pathophysiology, Heidelberg University, Heidelberg, Germany, 2Medical Clinic V, University Hospital Mannheim, Heidelberg University, Mannheim, Germany

• NFAT5 is identified as a mechanosensitive tran-scription factor promoting responses of vascular smooth muscle cells biomechanical stress.

• Loss of NFAT5 impairs expression of transcripts controlling cell cycle, cytoskeletal dynamics, cel-lular adhesion and transcription/translation.

• SMC-restricted loss of NFAT5 in mice impairs vascular smooth muscle cell proliferation during arteriogenesis and hypertension-induced hyper-trophy of the arterial wall.

T063

The role of Tie1 receptor in meningeal lym-phatic vessel development and function in inflammation

Emilia Korhonen1, Zhilin Li1, Eleonoora Wihuri1, Salli Antila1, Kari Alitalo1

1Wihuri Research Institute / University of Helsinki, Helsinki, Finland

• Tie1 is necessary for the growth and maturation of meningeal lymphatic vessels

• Lymphatic endothelial cell-specific Tie1 defi-ciency reduces EAE severity

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IVBM2018

T064

Microvascular blood flow kinetics represent a novel treatment target for critical ischemia

Santeri Tarvainen1,2, Olli Hautero3, Kari Kalliokoski3,4, Tanja Tarvainen3,4, Galina Wirth1, Jouni Taavitsainen1, Jarkko Hytönen1, Tuomas Selander2, Tomi Laitinen2, Harri Hakovirta3, Juhani Knuuti3,4, Kimmo Mäkinen2, Seppo Ylä-Herttuala1,2, Petra Korpisalo1,2,4

1University Of Eastern Finland, Kuopio, Finland, 2Kuopio University Hospital, Kuopio, Finland, 3Turku University Hospital, Turku, Finland, 4Turku PET Centre, Turku, Finland

• Despite necrosis or rest pain, resting blood flow is normal in critically ischemic human legs.

• Instead, both capillary structure and microvascu-lar blood flow kinetics are significantly altered in the ischemic muscles.

• Altered microvascular blood flow kinetics may thus represent a novel treatment target for crit-ical ischemia.

T065

Diastolic hypertension, albuminuria, adverse cholesterol profiles, dysregulated hepato-renal cells indicated declined cAMP-related defense potency

Ruth-Maria Korth1

1Allgemeinmedizin Fida, Munich, Germany

• Diastolic hypertension and albuminuria over-lapped with self-reported critical alcohol con-sumption (about 30±9g ethanol/day, 33% of 131).

• The majority of men with dyslipidemia reported heavy alcohol consumption (Alb/Trig:22±9, LDL/HDL-C:3.5±1, VLDL-C:46±16>30 mg/dl, 54±10g ethanol/day, 13% of 131, 46±13 years).

• The majority of late alcohol abusers had pro-teinuria/hematuria, high hepatic GGT, diabetes, hypertension (3.7±0.3mmo/l, 15% of 131).

T066

Endothelial-dependent mechanisms of aortic valve calcification

Aleksandra Kostina1, Daria Semenova1, Olga Irtyuga1, Anna Kostareva1, Anna Malashicheva1

1Almazov National Medical Research Centre, Saint-Petersburg, Россия

• Endothelial signaling is critical in aortic valve cal-cification

• Activated Notch increases osteogenic differentia-tion of aortic valve interstitial cells

• Dysregulated Notch is involved in aortic valve cal-cification

T067

The RING ligase complex Cullin-3-Rbx1-KCTD10 controls endothelial barrier function through K63-specific ubiquitination of RhoB

Igor Kovacevic1, Tomohisa Sakaue2,3,4, Jisca Majolee1, Manon Pronk1, Masashi Maekawa2,3,4, Dirk Geerts5, Mar Fernandez-Borja6, Shigeki Higashiyama2,3,4, Peter Hordijk1

1Department of Physiology, VUMC, Amsterdam, Netherlands, 2Division of Cell Growth and Tumor Regulation, Proteo-Science Center (PROS), Ehime University, Toon, Japan, 3Department of Cardiovascular and Thoracic Surgery, Ehime University Graduate School of Medicine, Toon, Japan, 4Department of Biochemistry and Molecular Genetics, Ehime University Graduate School of Medicine, Toon, Japan, 5Department of Pediatric Oncology/Hematology, Erasmus University Medical Center, Rotterdam, Netherlands, 6Department of Molecular Cell Biology, Sanquin Research Amsterdam, Amsterdam, Netherlands

• RhoB and RhoA share 85% sequence identity, but RhoB is rapidly degraded in endothelial cells, in contrast to RhoA which si more stable.

• In endothelial cells KCTD10-Cullin-3-Rbx1 com-plex ubiquitinates RhoB which drives lysosomal localization and degradation of RhoB.

• In inflammatory conditions RhoB expression is rapidly increased which results in disruption of endothelial barrier.

T068

Extracellular matrix proteins modulate the basal and induced expression of inflammatory cytokines in endothelial cells

Abby Callahan2, Laura Rossi3, Tom Kovala1,2

1Division of Medical Sciences, Northern Ontario School Of Medicine, Sudbury, Canada, 2Department of Biology, Laurentian University, Sudbury , Canada, 3Department of Biology, Nipissing University, North Bay, Canada

• Sphingosine 1-phosphate (S1P) and vascular endothelial growth factor (VEGF) induce expres-sion of the proangiogenic, proinflammatory cyto-kines IL-6, CXCL8 and CCL2.

• Growth of HUVECs on specific extracellular matrix proteins modulated both the basal and induced expression of the individual cytokines.

• While the expression of the cytokines required activation of NF-kB, constitutive activation of JAK-STAT pathways were also necessary

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IVBM2018

T069

MHCII-mediated Antigen-presentation by Lymphatic Endothelial Cells in Experimental Autoimmune Encephalomyelitis

Camille Kowalski1, Marion Humbert1, Stephanie Hugues1

1Unige Faculty Of Medicine, Geneva, Switzerland

• Use of genetically modified “MOG35-55 LEC” mice, in which MOG35-55 peptide is specifically presented by lymphatic endothelial cells (LEC) through MHCII molecules

• MOG35-55 LEC mice exhibited a significant EAE attenuation

• LECs could contribute to the tolerization of anti-gen-specific CD4+ T cells.

T070

Folic Acid Exerts Post-Ischemic Neuroprotec-tion In Vitro Through HIF-1α Stabilization

Charles Kozhikkadan Davis1, Rajanikant G.K.1

1National Institute of Technology Calicut, Calicut, India

• Folic acid bound to proteins, PHD2, FIH and pVHL alike in silico studies.

• Folic acid provided neuroprotection following oxygen-glucose deprivation in vitro.

• Folic acid promoted angiogenesis ex ovo.

T071

The role of long noncoding RNA Meg8 in endothelial cell function

Veerle Kremer1,2, Eva van Ingen3, Laura Stanicek1, Yaël Nossent3, Reinier Boon1,4

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, Netherlands, 2Department of Medical Chemistry, Academic Medical Center Amsterdam, Amsterdam, Netherlands, 3Department of Surgery, The Netherlands Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center, Leiden, Netherlands, 4Institute of Cardiovascular Regeneration, Goethe University, Frankfurt am Main, Germany

• The 14q32 locus of the human genome contains non-coding RNAs shown to be regulated during ischemic disease.

• Silencing of Meg8, found on 14q32, impairs endothelial function, angiogenesis and induces senescence.

• Meg8 is thought to be involved in barrier func-tion by regulating junction proteins.

T072

Endothelial-Mesenchymal-Transition (EndMT) contributes to Intimal Hyperplasia and is gov-erned by TGFβ, MAPK7 and microRNAs.

Byambasuren Vanchin1, Martin C. Harmsen1, Jan-Renier A.J. Moonen1, Guido Krenning1

1University Medical Center Groningen, Groningen, Netherlands

• Endothelial-Mesenchymal-Transition contributes to intimal hyperplasia.

• Biomechanical forces modulate pro- and antiath-erogenic signaling pathways in endothelial cells.

• The TGFb-miR-374b-axis inhibits atheroprotec-tive pathways in endothelial cells.

T073

Endothelial-specific deletion of Tgfbr2 reduces tumorigenesis and modulates angio-genesis in pancreatic neuroendocrine tumors

Ewa Kurzejamska1, Nikolas Eleftheriou1, Eugenia Cordero1, Kristian Pietras1

1Faculty of Medicine, Department of Laboratory Medicine, Division of Translational Cancer Research, Lund University Cancer Center at Medicon Village, Lund, Sweden

• Endothelial-specific deletion of Tgfbr2 in pancre-atic neuroendocrine tumors results in:

• Reduced number of angiogenic islets, tumor number and volume

• Disorganized and poorly defined vessel pheno-type with more junctions and longer vessels

• Increased number of inflammatory cells in the tumors.

T074

Association between choroidal macrophages and perivascular mural cells and their influ-ence in choroidal pathology

Anil Kumar1, Zhen Xiong1, Wanhong Li1, Xuri Li1

1Laboratory of Ocular Neurovascular Biology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou , China

• Resident macrophages demonstrate extensive physical interactions with PMCs. These interac-tions occur constitutively and may regulate vas-cular structure and function.

• Alterations in macrophage polarization in retinal and choroidal disease may influence pericyte density, survival and function.

• Changes in macrophage-PMC interactions, sec-ondary to macrophage polarization, may be related to choroidal changes in AMD progression.

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IVBM2018

T075

Positive correlation of serum resistin level with artery stiffness in patients with chronic kidney disease

Chiu-Huang Kuo1, Chih-Hsien Wang1, Yu-Li Lin1, Yu-Hsien Lai1, Bang-Gee Hsu1,2

1Division of Nephrology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan, 2School of Medicine, Tzu Chi University , Hualien, Taiwan

• Serum resistin level is positively associated with aortic arterial stiffness in patients with chronic renal kidney disease.

• Serum resistin level is positively associated with carotid-femoral pulse wave velocity values in chronic renal kidney disease patients.

T076

Serum adipocyte fatty acid binding protein is positively associated with pulse wave velocity in hemodialysis

Chiu-Huang Kuo1, Chih-Hsien Wang1, Yu-Li Lin1, Yu-Hsien Lai1, Bang-Gee Hsu1,2

1Division of Nephrology, Buddhist Tzu Chi General Hospital, Hualien, Taiwan, 2School of Medicine, Tzu Chi University , Hualien, Taiwan

• Serum adipocyte-fatty-acid-binding protein level is the independent predictor of aortic artery stiff-ness in hemodialysis patients.

• Serum adipocyte-fatty-acid-binding protein is positively associated with carotid-femoral pulse wave velocity values in hemodialysis patients.

T077

5-methoxytryptophan (5-MTP) protects against high-fat diet-induced atherosclerosis and vascular calcification in ApoE-deficient mice

Cheng-chin Kuo1

1Institute Of Cellular And System Medicine, National Health Research Institutes, , Taiwan

• High-fat diet (HFD) diminished vascular cell 5-MTP level in the atherosclerotic lesions of ApoE-/-.

• 5-MTP administration prevents HFD-induced serum IL-6 and lipid accumulation and calcifi-cation in the atherosclerotic lesions of ApoE-/- mice.

• 5-MTP inhibits VSMC migration, chondrogenic differentiation, and calcification via suppressing IL-6-mediated RANKL induction signaled by p38 signaling in VSMCs.

T078

Mechanisms governing microRNA regulation in atherogenesis

Suvi Kuosmanen1, Maria Bouvy-Liivrand2, Ana Hernández de Sande2, Pierre Moreau1, Henri Niskanen1, Merja Heinäniemi2, Anna-Liisa Levonen1, Minna Kaikkonen-Määttä1

1A.I.V. Institute, University Of Eastern Finland, Kuopio, Finland, 2School of Medicine, University of Eastern Finland, Kuopio, Finland

• MicroRNA (miRNA)-related processes were inves-tigated in human endothelial cells under various pro-atherogenic stimuli by obtaining and integrat-ing next-generation sequencing data,

• This integrative approach allowed us to establish several regulatory networks among co-regulated miRNAs and target genes,

• Here, we present evidence for a regulatory net-work of miR-93, NRF2, KLF2, PFKFB3, VEGFA, FOXO1 and MYC.

T079

Specific inhibition of bromodomain-containing protein 4 decreases experimental pulmonary hypertension

Konda Babu Kurakula1, Diederik van der Feen2, Harm Jan Bogaard3, Rolf Berger2, Sebastien Bonnet4, Marie Jose Goumans1

1Leiden University Medical Center, Leiden, Netherlands, 2UMCG, Groningen, Netherlands, 3VUMC, Amsterdam, Netherlands, 4Laval University, Quebec, Canada

• Inhibition of BRD4 decreases proliferation, inflammation of pulmonary vascular cells via inhibition of TGFb pathway in pulmonary arterial hypertension (PAH)

• Inhibition of BRD4 attenuates vascular remodel-ling in vivo

• Blocking BRD4 activity improves right ventricle function in PAH

Posters – Tuesday

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IVBM2018

T080

Proinflammatory phenotype of LSEC is not linked with their defenestration in mice fed high-fat diet

Edyta Kus1, Patrycja Kaczara1, Izabela Czyżyńska-Cichoń1, Karolina Szafranska1, Bartosz Zapotoczny1, Mrs. Agnieszka Kij1, Agnieszka Sowinska2, Jerzy Kotlinowski1, Lukasz Mateuszuk1, Jolanta Jura1, Elżbieta Czarnowska2, Marek Szymoński1, Stefan Chlopicki1

1Jagiellonian University, Krakow, Poland, 2The Children’s Memorial Health Institute, Warszawa, Poland

• We revisited the relationship between LSEC proinflammatory response, defenestration and impairment of LSEC’s bioenergetics during NAFLD

• LSEC fenestrations and bioenergetics are func-tionally preserved despite metabolic and proin-flammatory burden linked to HFD

• LSEC shows structural and metabolic adaptive capacity that might mitigate NAFLD progression

T081

MDM2 induces vascular calcification through its E3 ligase activity

Duk-hwa Kwon1, MS Nakwon Choe1, Sera Shin1, Yoonseok Nam1, Hosouk Joung1, Geon Jeong1, Juhee Ryu1, Gwang Hyeon Eom1, Nacksung Kim1, Young-kuk Kim1, Jae-Taek Kim2, Woo Jin Park3, Susan M. Mendrysa4, Hyun Kook1

1Chonnam National University Medical Center, , South Korea, 2College of Medicine, Chung-Ang University, , South Korea, 3Gwangju Institute of Science and Technology, , South Korea, 4College of Veterinary Medicine, Purdue University, , USA

• VSMC-specific genetic ablation of MDM2 blunted the vitamin D3-induced VC

• VSMC-specific transgenic overexpression of MDM2 wild type (WT), but not Y489A nor a dR, induced VC

• E3 ligase-activity is required for MDM2-induced VC

T082

Vascular regeneration through the reprogram-ming of human fibroblasts by plant stem cell extracts

Yoo-Wook Kwon1, Kyung Woo Park1, Hyun-Jai Cho1, Hyo-Soo Kim1

1Seoul National University Hospital, , South Korea

• Plant stem cell (callus)-derived proteins could reprogram human fibroblasts.

• We observed reprogramming activities of plant callus extract on human dermal fibroblast. Here, we demonstrate molecule ‘S’, major component of Sequoiadendron Giganteum callus extract, reprogrammed somatic fibroblast to Mesodermal and Ectodermal precursor cells.

• The change of gene expression by ‘S’ might be regulated by epigenetic modification including promoter methylation.

T083

CLEC14A in regulation of VEGFR-dependent signals in the vasculature

Young-guen Kwon1

1Yonsei University, , South Korea

Posters – Tuesday

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IVBM2018

T084

Platelet-derived calpain cleaves the endothe-lial protease-activated receptor 1 and medi-ates vascular inflammation in diabetes

Anastasia Kyselova1,2, Amro Elgheznawy1,2, Ilka Wittig3, Juliana Heidler2,3, Alexander W. Mann4, Wolfram Ruf2,5,6, Ingrid Fleming1,2, Voahanginirina Randriamboavonjy1,2

1Institute For Vascular Signalling, Centre of Molecular Medicine, Goethe University, Frankfurt am Main, Germany, 2German Center of Cardiovascular Research (DZHK), Partner site Rhein-Main, Frankfurt am main, Germany, 3Functional Proteomics, SFB 815 Core Unit, Goethe University, Frankfurt am Main, Germany, 4Endokrinologikum Frankfurt, Frankfurt am Main, Germany, 5Center for Thrombosis and Hemostasis, University Medical Center, , Germany, 6Department of Immunology and Microbiology, the Scripps Research Institute, La Jolla, USA

• Calpain carried by platelet-derived microparticles target the protease-activated receptor 1 on the endothelial cell surface to initiate vascular inflam-mation.

• Levels of the soluble endothelial protein C recep-tor directly correlate with plasma calpain activity and may serve as promising biomarker.

• Calpain inhibition is a new approach to prevent diabetes-associated vascular inflammation.

T085

Crosstalk of Signaling Pathways in Angiogen-esis: VEGF, Erbb and Vascular Malformations

Suvi Jauhiainen1, Pia Vuola2, Henna Ilmonen1, Sara Keränen1, Minna U. Kaikkonen1, Jouko Lohi3, Anne Pitkäranta4, Seppo Ylä-Herttuala1, Johanna P. Laakkonen1

1A.I. Virtanen Institute, University Of Eastern Finland, Kuopio, Finland, 2Department of Plastic Surgery, Helsinki University Central Hospital, Helsinki, Finland, 3Department of Pathology, HUSLAB, Helsinki University Hospital, Helsinki, Finland, 4Department of Pediatric Surgery, Children’s Hospital, Helsinki University Hospital, Finland

• Perturbation of VEGF signaling is linked to most benign vascular tumors and vascular malforma-tions.

• We show crosstalk of VEGF and Erbb signaling pathways and discuss of their role in vascular malformations.

• Based on knowledge of cellular mechanisms, novel treatment strategies can be developed for vascular anomalies that are inoperable or do not respond to sclerotherapy.

T086

PI3Kγ-dependent T cell response delays endothelial healing and reveals a novel role for arterial CXCL10.

Muriel Laffargue1, Adrien Lupieri1, Natalia Smirnova1, Romain Solinhac1, Nicole Malet1, Lynda Zeboudj2, Hafid Ait Oufella2, Emilio Hirsch3, Paul Phayon1, Thibault Lhermusier1, Didier carrié1, Jean-Francois Arnal1, Damien Ramel1, Stephanie Gayral1

1Department of Vascular Biology of the Institute of Metabolic and Cardiovascular Diseases (I2MC), Université de Toulouse 3, INSERM UMR1048 , Toulouse, France, 2Paris - Cardiovascular Research Center (PARCC), Université Paris Descartes, Sorbonne Paris Cité, INSERM UMR970, Paris, France, 3Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Torino, Italy

• PI3Kγ-dependent T cell response is involved inblockadeofarterialhealing.

• SMCactsasarelaybetweenTcellsandendothe-lialcellsininflammatoryconditionsthroughthesecretionofCXCL10

• CXCL10directly acts on arterialwall to preventcorrectendothelialhealing

T087

A super-enhancer mediates endothelial-spe-cific gene expression.

Nihay Laham Karam1, Isidore Mushiyimana1, Henri Niskanen1, Minna Kaikkonen1, Seppo Ylä-Herttuala1,2,3

1A.I. Virtanen Institute, University Of Eastern Finland, Kuopio, Finland, 2Heart Center, Kuopio University Hospital, Kuopio, Finland, 3Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• We aimed to identify and characterise a super-en-hancer that could induce endothelial specific gene expression.

• We screened 20 super-enhancers and identi-fied one that activated a minimal promoter and consequently reporter expression specifically in endothelial cells.

• This super-enhancer was activated by hypoxia, it interacted with specific cellular gene promoters and would be useful for angiogenesis targeted therapeutic vectors.

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IVBM2018

T088

Jumping over the barrier: novel treatment strategies for angiotropic glioma eradication

Vadim Le Joncour1, Maija Hyvönen1, Pauliina Filppu1, Pauliina S. Turunen2,5, Harri Sihto1, Michael Weller3, Jessica Rosenholm4, Kaisa Lehti2,5, Jukka Westermarck6, Pirjo Laakkonen1

1Research Programs Unit, Translational Cancer Biology, University of Helsinki, Helsinki, Finland, 2Department of Microbiology, Tumor and Cell Biology (MTC) Karolinska Institutet, Stockholm, Sweden, 3Department of Neurology and Brain Tumor Center, University Hospital Zurich and University of Zurich, Zurich, Switzerland, 4BioNanoMaterials research group, Åbo Academy University, Turku, Finland, 5Research Programs Unit, Genome-Scale Biology, University of Helsinki, Helsinki, Helsinki, Finland, 6Finnish Cancer Institute, Turku Center for Biotechnology , Turku, Finland

• Glioma is an incurable disease and drugs are chal-lenged by the sheltering effect of the BBB and highly invasive cells.

• We developed an artificial BBB to screen nano-compounds diffusion and glioma targeting. We also discovered an unexpected sensitivity of tumor cells towards the lysosomal damage (LMP).

• Patient avatars have been used to validate the nanoparticles and LMP-inducing agents efficacy.

T089

Decreased expression of Flt-1 contributes to the pathogenesis of Hereditary Hemorrhagic Telangiectasia 2

Jérémy.H Thalgott1, Damien Dos-Santos-Luis2,3, Anna.E Hosman4, Sabrina Martin2,3, Noël Lamandé2,3, Diane Bracquart2,3, Samly Srun2,3, Hetty de Boer1, Steven Kroon4, Repke.J Snijder4, Frans Disch4, Yihai Cao5, Hans-Jurgen J Mager4, Ton Rabelink1, Christine L Mummery6, Karine Raymond6, Franck Lebrin1,2,3,7

1Einthoven Laboratory for Experimental Vascular Medicine, Department of Internal Medicine, Leiden University Medical Center, Leiden, Netherlands, 2CNRS UMR 7241, INSERM U1050, Collège de France, Paris, France, 3MEMOLIFE Laboratory of Excellence and PSL Research University, Paris, France, 4St. Antonius Hospital, Nieuwegein, The Netherlands, 5Department of Microbiology, Tumor and Cell Biology, Karolinska Institute, Stockholm, Sweden, 6Department of Anatomy and Embryology, Leiden University Medical Center, Leiden, The Netherlands, 7CNRS UMR 7587, INSERM U979, Institut Langevin, ESPCI, Paris, France

• Vascular genetic disease• Angiogenesis• VEGF signalling

T090

Secreted frizzled-related protein 5 restores WNT5A-induced impaired vasorelaxation and acts as a compensatory factor

Yun Kyung Cho1, u Mi Kang1, Seung Eun Lee1, Yoo La Lee2, So Mi Seol2, Cheol-Young Park3, Jaetaek Kim4, Woo Je Lee1, Joong-Yeol Park1, Chang Hee Jung1

1Department of Internal Medicine, Asan Medical Center, University of Ulsan College of Medicine, , South Korea, 2Asan Institute of Life Sciences, Asan Medical Center, University of Ulsan College of Medicine, , South Korea, 3Department of Internal Medicine, Sungkyunkwan University School of Medicine, Kangbuk Samsung Hospital, , South Korea, 4Department of Internal Medicine, Chung-Ang University Hospital, , South Korea

• Secreted frizzled-related protein 5 (SFRP5) is an endogenous inhibitor of WNT5A signaling and an emerging anti-inflammatory adipokine.

• In vitro and ex vivo studies demonstrated that SFRP5 exerted a vasorelaxant function by antag-onizing the WNT5A/JNK pathway.

• In subjects with type 2 diabetes mellitus (T2D), the circulating SFRP5 level was positively asso-ciated with brachial-ankle pulse wave velocity (baPWV).

T091

Comparison of angiogenic activities of three neuropeptides, substance p, secretoneurin, and neuropeptideY in myocardial infarction

jaeyeon Lee1,2, Mirim Kim1,2, Myeongjin Song1, Yongdoo Park1

1Department of Biomedical Engineering, College of Medicine, Korea University, Seoul, South Korea, 2These authors contributed equally to this work, ,

• Using smart hydrogel immobilized neuropeptides• Neuropeptides have a positive impact on angio-

genesis• Neuropeptides especially substance P improve

the cardiac function of heart disease model

T092

Organ-on-a-chip 3D co-culture platform fab-ricated capillary force guided patterning and injected molding methods

Byungjun Lee1,2, Younggyun Lee2, Jihoon Ko2, Suryong Kim2, Somin Lee2, Noo Li Jeon1,2

1Cruiochips inc., South Korea, 2Seoul National University, South Korea

• 3D Liquid and hydogel patterning • In vitro miniaturized vasculogenesis platform• Organ-on-a-chip technology

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IVBM2018

T093

Endothelial-specific Akt1 deficiency enhances atherosclerotic plaque progression

Monica Lee1, Ana Gamez Mendez1, Binod Aryal1, Noemi Rotllan1, Carlos Fernandez-Hernando1, William Sessa1

1Yale University, New Haven, United States

• Endothelial Akt1 expression promotes an athero-protective environment

• Vascular susceptibility to inflammatory events is likely modulated through endothelial PI3K/Akt activity

• Adult, endothelial-targeted Akt1 deletion com-bined with a high cholesterol diet promotes sys-temic IFNγ production

T094

Vascular regeneration with engineered humanpluripotent stem cell-derived endothe-lial cells

Shin-Jeong Lee1, Young-sup Yoon2

1Yonsei University, Seoul, South Korea, 2Emory University, Atlanta, USA

T095

Therapeutic effects of engineered human plu-ripotent stem cell-derived lymphatic endothe-lial cells on experimental lymphedema

Shin-Jeong Lee1, Dongchan Son1, Cholomi Jung1, Ho-Wook Jun3, Young-sup Yoon1,2

1Yonsei University, Seoul, South Korea, 2Emory University, Atlanta, USA, 3UAB, Alabama, USA

T096

In vivo visualization of chronic neuroinflamma-tion in chemical-induced mouse model

Jingu Lee1, Eunji Kong1, Pilhan Kim1

1Korea Advanced Institute of Science Technology, Daejeon 34141, South Korea

• Chronic neuroinflammation could cause recruit-ment of leukocytes to the brain within a week.

• Distributions of leukocytes in brain parenchyma were changed over several weeks.

• Circulating leukocytes interacted with damaged neurovascular unit.

T097

Visualization and quantification of pericyte incorporated 3D in vitro angiogenesis

Eujin Lee1, Haruko Takahashi1, Joris Pauty1,2, Maki Kabara3, Jun-ichi Kawabe3, Yukiko Matsunaga1,2

1CIBiS, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan, 2LIMMS/CNRS-IIS UMI 2820, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan, 3Department of Cardiovascular Regeneration and Innovation, Asahikawa Medical University, Hokkaido, Japan

• Pericytes that surround the endothelial cell layer are considered to be important in angiogenesis, but how they behave remains poorly understood

• 3D endothelial cell and pericyte co-culture microvessel model was constructed to visualize interactions between endothelial cells and peri-cytes

• Presence of pericytes prevented pre-existing ves-sel expansion and enhanced sprout formation and elongation

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IVBM2018

T098

Vascular abnormalizing factor Sox7 deter-mines the therapeutic efficacy of VEGFR2 inhibition in high-grade glioma

Eunhyeong Lee1, Il-Kug Kim2, Jee Myung Yang3, Seungjoo Lee4, Injune Kim1,3

1Biomedical Science and Engineering Interdisciplinary Program, Korea Advanced Institute of Science and Technology, Daejeon, South Korea, 2Department of Plastic and Reconstructive Surgery, Seoul National University Hospital, Seoul, South Korea, 3Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology, Daejeon, South Korea, 4Department of Neurosurgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, South Korea

• Sox7-VEGFR2 axis promotes high-grade glioma growth via vessel abnormalization.

• VEGFR2 inhibition induces opposite glioma response depending on the Sox7 level.

• Endothelial Sox7 predicts poor prognosis and impaired vasculatures in high-grade glioma.

T099

The role of TNF-a-induced PGD2 in pheno-typic conversion of VSMCs via ERK signaling pathway

Hye Sun Lee1, Jung Min Ha1, Seo Yeon Jin1, Farzaneh Vafaeinik1, Seo Jin Maeng1, Hye Jin Kum1, Yoo Jin Jung1, Sun Sik Bae1

1Pusan National University School Of Medicine, Yangsan-si, South Korea

• TNF-α strongly induced the phenotypic change of VSMCs.

• COX2-mediated PGD2 production was controlled by TNF-a.

• PGD2 may act as the key regulator of dedifferen-tiation and it acts new receptor of TNF-α-induced PGD2 in VSMC dedifferentiation.

T100

3D Perfusable Vasculature Model on Injection Molded Chip for Multi-Application

Somin Lee1, James Yu1, Jungeun Lim2, Younggyun Lee2, Byungjun Lee2,3, Noo Li Jeon1,2,3

1Program for Bioengineering, Seoul National University, Seoul, South Korea, 2Mechanical Engineering, Seoul National University, Seoul, South Korea, 3Curiochips Inc., Seoul, South Korea

• Human cell based 3D microfluidic in vitro model• 3D model of perfusable vasculature formed by in

vivo like vasculogenesis• Vascular model optimized for diverse develop-

mental and pathological research

T101

RPE-Choroid Complex Microfluidic Model for Choroidal Neovascularization(CNV) Pathogen-esis Research

Somin Lee1, Minhwan Chung1, Byung Joo Lee2, Kyungmin Son1, Byungjun Lee1, Noo Li Jeon1, Jeong Hun Kim2

1Seoul National University, Seoul, South Korea, 2Seoul National University Hospital, Seoul, South Korea

• 3D in vitro human cell based organotypic vascu-lature model mimicking RPE-choroid compex in outer blood-retinal barrier(BRB)

• Retinal pigment epithelium(RPE) layer was recon-stituted in the model having physiological barrier function and polarized protein expression

• Pathological condition mimicking choroidal neo-vascularization(CNV) was established and com-mercial drug, bevacizumab, was tested for verify-ing eligibility in drug development

T102

Normalization of tumor vasculature using anti-vascular-inflammation nanoparticles inhibits tumor progression and metastasis

Young Sun Choi1, Soo Hyun Kang1, Li Kang1, Yun Ge1, Jong Sup Bae1, In San Kim2, You Mie Lee1

1BK21 Plus Multi-Omics Based Creative Drug Research Training Team (22A20154413076), Research Institute of Pharmaceutical Sciences, College of Pharmacy, South Korea, 2Biomedical Research Institute, KIST, Seoul, South Korea

• Anti-vascular-inflammation nanoparticles, TFG and TFMG were genetically engineered fer-ritin-based protein nanocages comprising EPCR-targeting peptides (PC-Gla) and PAR-1-acti-vating peptides (TRAP).

• TFG and TFMG inhibited tumor growth and metastasis in LLC allograft and MMTV-PyMT breast cancer models.

• TFG and TFMG normalized the abnormal tumor vasculature, with significantly improved pericyte coverage reduced hypoxic regions, and enhanced effect of chemotherapeutic agent.

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IVBM2018

T103

ACVR2B-Fc protects myocardium from acute ischemia-reperfusion injury

Johanna Magga1,2, Laura Vainio1, Ruizhu Lin1,3, Juha Hulmi4,5, Markus Räsänen6, Zoltan Szabo1, Saija Taponen1, Erhe Gao7, Mika Laitinen8, Arja Pasternack5, Kari Alitalo6, Riikka Kivelä6, Olli Ritvos5, Risto Kerkelä1,3

1Research unit of Biomedicine, University of Oulu, Oulu, Finland, 2Biocenter Oulu, University of Oulu, Oulu, Finland, 3Medical Research Center, Oulu University Hospital, Oulu, Finland, 4Neuromuscular Research Center, University of Jyväskylä, Jyväskylä, Finland, 5Department of Physiology, University of Helsinki, Helsinki, Finland, 6Wihuri Research Institute and Translational Cancer Biology Program, University of Helsinki, Helsinki, Finland, 7Center for Translational Medicine, Temple University School of Medicine, Philadelphia, USA, 8Department of Medicine, University of Helsinki and Helsinki University Hospital, Helsinki, Finland

• Systemic blockade of activin ACVR2B receptor ligands by ACVR2B-Fc protects myocardium in ischemia-reperfusion injury.

• ACVR2B ligand myostatin exacerbates hypoxic stress, which is alleviated by ACVR2B-Fc in cardio-myocytes.

• ACVR2B-Fc reduces cardiomyocyte death and proteolytic pathways, induces hypertrophy and modifies cardiomyocyte metabolism for hypoxic conditions to protect the heart from isch-emia-reperfusion injury.

T104

Nrf2 deficiency impairs atherosclerotic lesion development but promotes unfavorable plaque phenotype in mice

Anna-Kaisa Ruotsalainen1, Jari Lappalainen1, Emmi Heiskanen1, Mari Merentie1, Virve Sihvola1, Simone Adinolfi1, Juha Näpänkangas2, Line Lottonen-Raikaslehto1, Emilia Kansanen1, ai Kaarniranta1, Seppo Ylä-Herttuala1, Matti Jauhiainen3, Eija Pirinen4, Anna-liisa Levonen1

1University Of Eastern Finland, Kuopio, Finland, 2University of Oulu, Oulu, Finland, 3Minerva Foundation Institute for Medical Research, Helsinki, Finland, 4University of Helsinki, Helsinki, Finland

• The effect of redox-active transcription factor Nrf2 on atherogenesis was studied in LDL recep-tor deficient (LDLR-/-) mice and LDLR-/- mice expressing apoB-100 only.

• The absence of Nrf2 reduced atherosclerotic lesion size in both models via systemic effects on lipid metabolism.

• Nrf2 deficiency in aged LDLR-/-ApoB100/100 mice led to a vulnerable plaque phenotype and increased plaque inflammation, predisposing to myocardial infarction.

T105

Pro-tumoral immune cell alterations in wild-type and Shb-deficient mice in response to 4T1 breast carcinomas

Xiujuan Li1,3, Kailash Singh1, Zhengkang Luo1, Mariela Mejia-Cordova1, Maria Jamalpour1, Björn Lindahl1, Ganlin Zhang2, Stellan Sandler1, Michael Welsh1

1Department of Medical Cell Biology, Uppsala University, Uppsala, Sweden, 2 Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala , Sweden, 3Cyrus Tang Hematology Center, Soochow University, Suzhou, China

• Absence of Shb increased 4T1 tumor lung metas-tasis although it did not affect tumor growth.

• Shb knockout tumors showed decreased redness and less developed vascular plexa located at the periphery of the tumors.

• 4T1 tumors alter immune cell responses that pro-mote tumor metastasis and immunologic escape in a Shb dependent manner.

T106

The role of PKN1/2 in vascular myogenic tone and smooth muscle differentiation

Rui Li1, Ramesh Chennupati1, Young-June Jin1, Lei Wang1, Nina Wettschureck1, Stefan Offermanns1

1Max Planck Institute For Heart And Lung, Bad Nauheim, Germany

• Smooth muscle cell (SMC) specific loss of PKN1 and PKN2 preserves arterial contractile responses but lead to a block of myogenic tone autoregula-tion.

• Ablation of PKN1/2 in smooth muscle cells did not affect basal blood pressure (BP) in mice but strongly reduced DOCA-salt induced hyperten-sion.

• Loss of PKN1/2 in SMCs attenuated dedifferen-tiation of SMCs during vascular remodeling pro-cesses.

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IVBM2018

T107

Novel function of VEGF-B in tethering the FGF2/FGFR1 pathway

Xuri Li1

1Zhongshan Ophthalmic Center, Guangzhou, China

• VEGF-B was discovered long time ago. However, its vascular effect and the mechanisms involved remain poorly understood.

• We recently found that VEGF-B can act as an endogenous inhibitor of the FGF2/FGFR1 path-way when they are highly expressed.

• Given the antiangiogenic nature of VEGF-B under conditions of high FGF2/FGFR1, caution is war-ranted when modulating VEGF-B activity for ther-apies.

T108

Modulation of erection by penile perivascular cells

Eduardo Linck Guimarães1, David O. Dias1, Daniel Holl1, Soniya Savant1, Evelina Vågesjö2, Mia Phillipson2, Christian Göritz1

1Department of Cell and Molecular Biology, Karolinska Institutet, Stockholm, Sweden, 2Department of Medical Cell Biology, Division of Integrative Physiology, Uppsala University, Uppsala, Sweden

• The penis presents a substantial number of peri-vascular cells, including a subpopulation express-ing the Sodium-dependent glutamate/aspartate transporter 1 (Glast).

• Expansion of Glast+ cell population induces long-lasting erections and exacerbated response to vasodilators. Optogenetic stimulation increases penile blood flow.

• Glast+ perivascular cell population is a novel cel-lular component of the erectile process and mod-ulator of penile blood flow.

T109

Ultrasound-derived local pulse wave velocity predicts ex vivo unloaded thickness in mouse carotid arteries

Benard Ogola1, Caleb Abshire1, Gabrielle Clark2, Kaylee Gentry1, Dylan Lawrence2, Margaret Zimmerman1, Kristin Miller2, Carolyn Bayer2, Sarah Lindsey1

1Tulane University, Department of Pharmacology, New Orleans, United States, 2Tulane University, Department of Biomedical Engineering, New Orleans, United States

• Because carotid-femoral pulse wave velocity is technically challenging, we determined whether measuring PWV within the carotid predicts arte-rial stiffness.

• Local carotid pulse wave velocity but not blood pressure correlated with ex vivo carotid wall thickness.

• Carotid pulse wave velocity may provide advan-tages over the currently accepted method.

T110

Rasip1 is a novel regulator for lymphatic ves-sel maintenance and lymphatic valve forma-tion

Xiaolei Liu1, Xiaowu Gu2, Wanshu Ma1, Michael Oxendine1, Hyea Jin Gil1, Ondine Cleaver2, Guillermo Oliver1

1Center for Vascular and Developmental Biology, Feinberg Cardiovascular Institute, Feinberg School of Medicine, Northwestern University, Chicago, United States, 2Department of Molecular Biology, University of Texas Southwestern Medical Cente, Dallas, United States

• Rasip1 is required for embryonic lymphatic vessel maintenance and lymphatic valve formation.

• Rasip1 regulates Cdc42 activity to regulate lym-phatic vessel junction integrity.

• Rasip1 is dispensable for postnatal lymphatic ves-sel maintanence but is required for pathological lymphangiogenesis, making it a potential thera-peutic target for lymphatic related diseases.

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IVBM2018

T111

Role of H3K27me3 histone demethylases in endothelial cell function

Oscar Liu1, Minna Kaikkonen-Määttä1

1A.I. Virtanen Institute For Molecular Sciences, University of Eastern Finland , Kuopio, Finland

• Knockdown of KDM4B and KDM6B resulted in 1.3 to 1.5-fold higher enrichment of H3K27me3 at selected regions around angiogenesis-related genes (VEGFA, PRDM1, CCL2 and CXCR4) under hypoxia.

• KDM-mediated demethylation of H3K27me3 is required for the expressions of angiogenesis-re-lated genes under hypoxia.

• Knockdown of selected KDMs affect endothelial cell proliferation and tube formations.

T112

Endothelial Dab1 Signaling Orchestrates Neu-ro-glia-vessel Communication in the CNS

Marta Segarra1, María R. Aburto1,2, Florian Cop1, Cecília Llaó-Cid1, Ricarda Haertl1, Miriam Damm1,2, Ioanna Bethani1, Marta Parrilla1,3, Anne Schänzer4, Hannah Schlierbach4, Till Acker4, Laura Mohr1, Matthias Ritter1, Amparo Acker-Palmer1,2,3

1Institute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Frankfurt am Main, Germany, 2Focus Program Translational Neurosciences (FTN), University of Mainz, Mainz, Germany, 3Max Planck Institute for Brain Research, Frankfurt am Main, Germany, 4Institute of Neuropathology, University of Giessen, Giessen, Germany

• Blood Brain Barrier• Corticogenesis• Developmental angiogenesis

T113

Overexpression of Calreticulin in endothelial cells changes insulin transcytosis

Tatiana Lobo1, Rajja Dalloul1, Nasrin Mesaeli1

1Weill Cornell Medicine Qatar, Doha, Qatar

• We hypothesized that overexpression of calretic-ulin reduce insulin transport to the target tissue due to onset of endothelial dysfunction.

• We used genetic approaches to overexpress cal-reticulin in vitro and in vivo.

• Our results illustrate that increased calreticulin expression in endothelial cells affect endothelial function, increase the vascular permeability and reduce the transcytosis of insulin through the endothelial cell of vasculature.

T114

Novel small molecule inhibitors of heme oxy-genase-1 exert anti-cancer activity in vitro

Paulina Podkalicka1, Olga Mucha1, Szymon Barwacz1, Kalina Andrysiak1, Anna Biela1, Szczepan Kruczek1, Maciej Mikulski2, Kamil Sitarz2, Michal Galezowski2, Arkadiusz Bialas2, Tomasz Rzymski2, Krzysztof Brzozka2, Alicja Jozkowicz1, Jozef Dulak1, Agnieszka Loboda1

1Jagiellonian University, Kraków, Poland, 2Selvita S.A, Kraków, Poland

• We initiated a drug discovery program aimed at the identification and characterization of small-molecule inhibitors of heme oxygenase-1 activity

• We identified compounds which inhibit the cata-lytic function of HO-1 at submicromolar concen-trations

• Our compounds exert antitumor effects in vitro including decreased viability, clonogenic poten-tial, migration and anti-angiogenic activity

T115

Endothelial progenitor cells improve right ven-tricular function in a model of chronic throm-boembolic pulmonary hypertension

Fanny Loisel1,2, Bastien Provost1, ulien Guihaire1,3, David Boulate1,4, Nassim Arouche2, Benoit Decante1, Peter Dorfmüller1,6, Elie Fadel1,4,5, Georges Uzan2, Olaf Mercier1,4,5

1INSERM UMR-S999 Marie Lannelongue Hospital, Le Plessis Robinson, France, 2INSERM UMR1197, Villejuif, France, 3Department of Cardiac Surgery Marie Lannelongue Hospital, Le Plessis Robinson, France, 4Department of Thoracic and Vascular Surgery and Heart-Lung Transplantation Marie Lannelongue Hospital, Le Plessis Robinson, France, 5Paris Sud University and Paris Saclay University, School of medicine , Kremlin Bicêtre, France, 6Department of pathology Marie Lannelongue Hospital, Le Plessis Robinson, France

• Coronary infusion of autologous endothelial pro-genitor cells improved right ventricular function in an animal model of chronic thromboembolic pulmonary hypertension

• Coronary infusion of autologous endothelial pro-genitor cells in the right ventricle resulted in a tendency to increased capillary density

• Coronary infusion of autologous endothelial pro-genitor cells in the right ventricle decreased car-diomyocyte surface area

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IVBM2018

T116

Endothelial cells cope with hypoxia-induced depletion of ATP via activation of cellular purine turnover

Karolina Losenkova1, Mariachiara Zuccarini1, Mikko Helenius1, Guillaume Jacquemet2, Evgenia Gerasimovskaya3, Camilla Tallgren1, Sirpa Jalkanen1, Gennady Yegutkin1

1MediCity Research Laboratory, University of Turku, Turku, Finland, 2Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland, 3Department of Pediatrics, University of Colorado Denver, Aurora, USA

• Acute hypoxia causes depletion of putative ATP stores in endothelial cells due to insufficient mitochondrial ATP synthesis.

• Acute hypoxia activates hydrolysis of extracellular nucleotides through the CD39-CD73 axis in endo-thelial cells.

• Acute hypoxia stimulates intracellular phospho-transfer networks responsible for extra-mito-chondrial ATP synthesis in endothelial cells.

T117

CMTM4 regulates angiogenesis by promoting cell surface recycling of VE-cadherin to endo-thelial adherens junctions

Laura Louzao Martinez1, Ihsan Chrifi2, Maarten M Brandt2, Christian GM van Dijk1, Petra E Burgisser2, Changbin Zhu3, Johan M Kros3, Marianne C Verhaar1, Dirk J Duncker2, Caroline Cheng1,2

1Department of Nephrology and Hypertension, UMC Utrecht, Utrecht, Netherlands, 2Department of Cardiology, Erasmus MC, Rotterdam, Netherlands, 3Department of Pathology, Erasmus MC, Rotterdam, Netherlands

• CMTM4 is essential for new vessel formation, both in vitro and in vivo.

• CMTM4 enhances the endothelial endocytic pathway and colocalizes with Rab4 and Rab7 pos-itive vesicles and with VE-cadherin.

• CMTM4 stimulates the internalization and rapid recycling of VE-cadherin and increases endothe-lial barrier function recovery.

T118

Differential pathways involved in the activa-tion of eNOS

Dominic Love1, Lena Claesson-Welsh1

1Uppsala University, Uppsala, Sweden

• eNOS alters vascular tone by affecting the vascu-lar smooth muscle cells through the production of NO. But little is known about its affect on the endothelial cells.

• Our evidence suggests that different ligand spe-cific pathways have different affects on endothe-lial cells.

• Depending on the activator of the eNOS pathway, different downstream affects are observed.

T119

The aging-regulated protein PNUTS is essen-tial for maintenance of endothelial barrier

Noelia Lozano-Vidal1, Laura Stanicek1,3, Christoph Dieterich2, Stefanie Dimmeler3,4, Reinier A. Boon1,3,4

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, Netherlands, 2Section of Bioinformatics and Systems Cardiology, Klaus Tschira Institute for Integrative Computational Cardiology, Department of Internal Medicine III, University Hospital Heidelberg, Heidelberg, Germany, 3Institute of Cardiovascular Regeneration, Goethe University, Frankfurt am Main, Germany, 4German Center for Cardiovascular Research (DZHK), Partner Site Rhein-Main, Berlin, Germany

• Phosphatase 1 Nuclear Targeting Subunit (PNUTS) is an aging-regulated gene. In HUVECs, PNUTS silencing impairs angiogenesis and endothelial barrier function.

• In vivo, endothelial-specific PNUTS KO mice pres-ent severe vascular leakage-related pathologies incompatible with life.

• PNUTS has an RNA-binding domain that inter-acts with and may regulate lncRNAs and mRNAs related with angiogenesis and endothelial cell-cell junctions and homeostasis.

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T120

CD93 in tumor angiogenesis and glioma development

Roberta Lugano1, Kalyani Vemuri1, Anna Dimberg1

1Uppsala University, Dept. of Immunology, Genetics and Pathology, Uppsala, Sweden

• CD93 deficiency delays GL261 tumor growth and improve mice survival

• CD93 regulates extracellular matrix organization in human endothelial cells and in GL261 glioma vasculature

• The vascular expression of CD93 correlates with increased fibronectin deposition in human gli-oma vessels

T121

IFNγ-Dependent Activation of Dermal Lym-phatic Vessels Limits Cytotoxic Immunity in Malignant and Inflamed Skin

Ryan Lane1, Julia Femel1, Alec Breazeale1, Christopher Loo1, Guillaume Thibault1, Andy Kaempf1, Motomi Mori1, Takahiro Tsujikawa1,2, Young Hwan Chang1, Amanda Lund1

1Knight Cancer Institute, Oregon Health & Science University, Portland, United States, 2Kyoto Prefectural University of Medicine, Kyoto City, Japan

• Lymphatic vessels express PD-L1 in response to antigen specific immunity in murine and human melanoma.

• Non-hematopoietic PD-L1 limits CD8+ T cell func-tion in tumor microenvironments.

• Lymphatic-specific insensitivity to IFNg boosts accumulation of intratumoral CD8+ T cells and local tumor control.

T122

SMAD2 and SMAD6: two novel genetic play-ers in aortic aneurysm and dissection.

Ilse Luyckx1, Elyssa Cannaert1, Aline Verstraeten1, Bart Loeys1

1University of Antwerp/Antwerp University Hospital, Antwerp, Belgium

• Loss-of-function mutations in SMAD2 cause syn-dromic aortic aneurysm and dissection, resem-bling Loeys-Dietz syndrome.

• SMAD6 loss-of-function mutations explain 2.5% of all bicuspid aortic valve related aortopathy cases and come with variable penetrance and phenotypical expression

• Transforming growth factor beta signaling is a key pathway in the pathogenesis of aortic and arterial aneurysm and dissection.

T123

Tuning the endothelial response: differential release of exocytic cargo from Weibel-Palade bodies.

Jessica McCormack1, Thomas Nightingale2, Christopher Robinson2, William Grimes1, Ian White1, Andrew Vaughan1, Louise Cramer1, Daniel Cutler1

1MRC Laboratory of Molecular Cell Biology, University College London, LONDON, United Kingdom, 2Centre for Microvascular Research, William Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, LONDON, United Kingdom

• Recruitment of an actin ring to exocytosing Wei-bel-Palade Bodies allows for differential release of von Willebrand Factor.

• Agonists have different abilities to recruit the ring, therefore the type of endothelial response will depend on the activating agonist(s).

• Failure to recruit the ring affects the conse-quences of exocytosis: vWF string production is inhibited, while leukocyte rolling is not.

T124

Melanoma cells use VLA-4 to intercalate into the tight blood brain barrier

Ruth Lyck1, Ana García-Martín1, Mitchell Levesque2, Ekkehard Hewer1

1University of Bern, Bern, Switzerland, 2University of Zürich, Zürich, Switzerland

• A tissue microarray from human biopsies revealed a majority of VLA-4 positive brain metastasis.

• To study the role of melanoma VLA-4 for breach-ing tight the blood brain barrier (BBB) we imaged (a) shear resistant arrest of melanoma cells and (b) intercalation over time.

• The mechanism of melanoma cell interaction with the BBB is different from T-cell extravasation.

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T126

Induced pluripotent stem cell derived endo-thelial cells display unique phenotype in low oxygen environments

Bria Macklin1,2, Sharon Gerecht1,2,3

1Department of Chemical and Biomolecular Engineering, Johns Hopkins University, BALTIMORE, United States, 2Institute for NanoBioTechnology, Johns Hopkins University, BALTIMORE, United States, 3Department of Materials Science and Engineering, Johns Hopkins University, BALTIMORE, United States

• “Hypoxic hydrogels” are generated by balancing oxygen diffusion with cellular oxygen consump-tion using collagen I.

• iPSC-ECs do not consume oxygen at similar levels of mature ECs.

• iPSC-ECs make more defined 3D networks in nor-moxic and “hypoxic” hydrogels as compared to mature ECs.

T127

Abnormal Lymphangiogenesis is Associated with Decreased Decidual Regulatory T Cells in Severe Preeclampsia

MD Yun Ji Jung1, MD Hayan Kwon2, Ja-Young Kwon1, Yong-sun Maeng1

1Yonsei University College Of Medicine, Seoul, South Korea, 2Dongguk University Ilsan Medical Center, Goyang-si, South Korea

• LYVE1-positive lymphatic vessels were abundance in decidua.

• In decidua of severe severe preeclampsia showed a low density and small diameter of LYVE1-posi-tive lymphatic vessels.

• Decreased lymphatic vessel density was cor-related with decreased number of decidual reg-ulatory T cells.

T128

Inhibition of Cullin ubiquitin ligase neddylation induces NFkappaB, RhoB and loss of endo-thelial barrier function

Jisca Majolee1, Manon C. A. Pronk1, Kinki K. Jim2, Jan S. M. van Bezu1, Astrid M. van der Sar2, Peter L. Hordijk1, I. Kovačević1

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, The Netherlands, Amsterdam, Netherlands, 2Department of Medical Microbiology and Infection Control, VU University Medical Center, Amsterdam, The Netherlands., Amsterdam, Netherlands

• A Cullin RING ligase deneddylation inhibitor was tested on HUVECs and in a zebrafish model for vascular leakage.

• Cullin deneddylation inhibition induced activation of the NFkB pathway and an increase in RhoB.

• Cullin activation induced endothelial barrier dis-ruption and increased macromolecule leakage in vitro and in vivo.

T129

Role of pacsin2 in junctional asymmetry, endothelial barrier stability and angiogenesis

Tsveta Malinova1, Ana Angulo1, Julian Nuchel2, Mariona Graupera3, Markus Plomann2, Stephan Huveneers1

1Department of Medical Biochemistry, Academic Medical Center, Amsterdam Cardiovascular Sciences, University of Amsterdam, Amsterdam, Netherlands, 2Center for Biochemistry, University of Cologne, Cologne, Germany, 3Vascular Signalling Laboratory, Institut d’Investigació Biomèdica de Bellvitge (IDIBELL), Gran Via de l’Hospitalet 199-203, 08908 L’Hospitalet de Llobregat, Barcelona, Spain

• Pacsin2 is recruited asymmetrically to remodel-ling endothelial cell-cell junctions directly after the dissociation p120-catenin – a regulator of VE-cadherin stability.

• At these junctional sites, pacsin2 recruits a down-stream effector which conducts asymmetric traf-ficking of VE-cadherin.

• In the vasculature of Pacsin2 and its effector knock-out mice, we detect a defect in the sprouts of forming retinal blood vessels.

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T130

RANTES-induced PKCα/PKC-δ balance regu-lates VE- cadherin and β-catenin phosphory-lation: role in monocyte transmigration

Hadjer Mamoune1, Loic Maillard1, Oualid Haddad1, Hanna Halawaty1, Olivier Oudar1, Nathalie Charnaux1,2, Angela Sutton1,2

1Inserm U1148 Lvts, Bobigny, France, 2APHP, Laboratoire de Biochimie, Hôpital Jean Verdier,, Bondy, France

• RANTES modifie endothelial cell to induce mono-cyte transmigration

• Monocyte transmigration RANTES-induced requires a fine regulation of the adherent junc-tions

• PKCα / PKCδ balance neatly regulates adherent junction proteins phosphorylation.

T131

Role of HMGB1 in vascular aging and calcifi-cation

Luigi Mancinelli1,2, Ileana Badi2, Filippo Zeni2, Filippo Taccia2, Andrea Silanos2, Claudio Saccu3, Rita Spirito3, Marco Bianchi4, Angela Raucci2

1Foundation IEO-CCM, Milan, Italy, 2Experimental Cardio-Oncology and Cardiovascular Aging Unit, CCM, Milan, Italy, 3Cardiovascular and Endovascular Surgery Unit, CCM, Milan, Italy, 4University Vita-Salute San Raffaele, Milan, Italy

• HMGB1 decreases in aged mouse aortas and during vascular smooth muscle cells (VSMC) senescence and calcification.

• HMGB1 negatively correlates with calcium depo-sition in aortas of uremic rats and human abdom-inal aortic aneurysm (AAA).

• HMGB1+/- mice show a modulation of calcium content in soft tissues compared to wild-type mice.

T134

Endothelial colony forming cell and extracel-lular matrix protein interaction in pulmonary arterial hypertension

Xue Manz1, Michael Floren2, Xiaoke Pan1, Kurt Stenmark2, Harm Jan Bogaard1, Robert Szulcek1

1Vu University Medical Center, Amsterdam, The Netherlands, 2Cardiovascular Pulmonary Research & Developmental Lung Biology Laboratories, University of Colorado, Denver, The United States of America

• Endothelial colony forming cells (ECFCs) from pulmonary arterial hypertension (PAH) patients show decreased adhesion on various extracellu-lar matrix (ECM) proteins, except for collagen III.

• ECFCs that adhered on ECM proteins show increased proliferation, suggesting an intrinsic proliferative dysfunction.

• Impaired ECFC-ECM interaction was illustrated by decreased number of focal adhesions.

T135

Chloride Intracellular Channel proteins func-tion in Sphingosine-1-phosphate signaling to regulate endothelial cell behavior

De Yu Mao1,2, Irina Jilishitz2,3, Matthew Kleinjan1, Sarah Lutz1, Yulia Komorova1, Timothy Hla3, Jan Kitajewski1,2

1University Of Illinois At Chicago, Chicago, United States, 2Columbia University Medical Center, New York, United States, 3Boston Children’s Hospital, Boston, United States

• CLIC1 and CLIC4 are critical for S1P-induced endothelial cellular responses and have non-re-dundant functions despite high sequence conser-vation.

• CLIC1 and CLIC4 are both required for S1PR1 receptor regulation of endothelial barrier integ-rity, migration and Rac1 activation.

• CLIC1 is required for S1P2 receptor regulation of endothelial actin stress fiber formation and RhoA activation.

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IVBM2018

T136

Extracellular matrix scaffolding: impact on vascular morphogenesis and endothelial mechanotransduction

Marion Marchand1, Claudia Umana1, Cathy Pichol-Thievend1, Romain Salza2, Sylvie Ricard-Blum2, Catherine Monnot1, Christophe Guilluy3, Laurent Muller1, Stéphane Germain1

1Center for Interdisciplinary Research in Biology, Collège de France, INSERM, CNRS, PSL Research University, Paris, France, 2Institut de Chimie et Biochimie Moléculaires et Supramoléculaires (ICBMS), UMR 5246 CNRS, Lyon, France, 3Institut Albert Bonniot, Grenoble, France

• LOXL2 associates with ECM proteins, collagen IV and fibronectin, intracellularly before direct incorporation in ECM filamentous structures

• LOXL2 regulates matrix scaffolding and stiffness at the endothelial cell surface

• LOXL2 regulates endothelial mechanotransduc-tion and vascular morphogenesis via scaffolding of the basement membrane

T137

New insights into mechanisms underlying PIK3CA-driven vascular malformations from genetic mouse models

Ines Martinez-Corral1, Taija Makinen1

1IGP department. Uppsala University, Sweden

• Genetic mouse models for PIK3CA-driven venous malformations (VM) and lymphatic malforma-tions (LM).

• Inducible models allow studying step-by-step development of the lesions.

• Lesions in the mouse models recapitulate fea-tures of human VM and LM.

T138

Detrimental effects of myeloid cell derived VEGF on cerebral vasculature in early isch-aemic stroke

Thomas Mathivet1,2, Claire Bouleti1, Antina De Boer3, Fabio Stanchi1, Marly Balcer1, Christian Stockmann2, Robin Lemmens3, Holger Gerhardt1,4

1Vascular Patterning Lab, Center for Cancer Biology, VIB, Leuven, Belgium, 2UMR 970, Paris Cardiovascular Research Center, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France, 3Laboratory of Neurobiology, Vesalius Research Center, VIB, Leuven, Belgium; Experimental Neurology (Department of Neurosciences) and Leuven Research Institute for Neuroscience and Disease (LIND), University of Leuven, Leuven, Belgium, 4Integrative Vascular Biology Laboratory, Max-Delbrück-Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany

• Vessel functional damages in early ischaemic stroke is accompanied by recruitment of myeloid cells.

• Recruitment of VEGF producing macrophages in the altered perivascular area, sustains vascu-lar leakage, edema formation and infarct area expansion.

• Depleting macrophages or their VEGF production protects blood vessel network and reduces neu-ronal cell death and so limit the infarct zone.

T139

Therapeutic Implications of Endothelial Het-erogeneity in Gliomas

Ken Matsumoto1, Florian Rambow2, Fabio Stanchi1, Thomas Mathivet1, Marly Balcer1, Jean-Christophe Marine2, Holger Gerhardt1

1Vascular Patterning Laboratory, Center for Cancer Biology, VIB/ KU Leuven, Leuven, Belgium, 2Laboratory for Molecular Cancer Biology, Center for Cancer Biology, VIB/ KU Leuven, Leuven, Belgium

• Using intravital imaging in mouse glioma model, we discovered unexpected progressive intratu-moural endothelial heterogeneity.,

• Cre-lox mediated fate mapping identified up to 10% of endothelial cells in progressive tumour stages that carry a non-endothelial and non-tu-moural lineage trace.,

• Ongoing studies indicate that these cells express typical endothelial markers and contribute to perfused and dynamically sprouting and remod-eling vessels.

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T140

Microvessel on a Chip for the Study of Anti-Angiogenic Drugs

Yukiko Matsunaga1,2,3, Joris Party1,2,3, Fabrice Soncin3,4

1CIBiS, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan, 2LIMMS/CNRS-IIS UMI 2820, Institute of Industrial Science, The University of Tokyo, Tokyo, Japan, 3CNRS/IIS/Centre Oscar Lambret/Université Lille 1 SMMiL-E project, Lille, France, 4Université Lille, CNRS, Institut Pasteur de Lille, UMR 8161, Lille, France

• In vitro model and organ-on-a-chip• The model allows to test effect of anti-angiogenic

drug• The model allows to visualize both angiogenic

sprouts and vascular permeability

T141

Bradykinin-induced relaxation of resistance arteries from residual CVD patients can involve NO-synthase, but not NO

Maximilian Matthies1, Maria Bloksgaard1, Lars Peter Riber3, Akhmadjon Irmukhamedov3, Jo G. R. De Mey1,2,3

1Department of Cardiovascular and Renal Research, Institute for Molecular Medicine, University of Southern Denmark, Odense, Denmark, 2Department of Pharmacology and Toxicology, Cardiovascular Research Institute Maastricht, Maastricht, the Netherlands, 3Department of Cardiac, Thoracic and Vascular Surgery, Odense University Hospital, Odense, Denmark

• The endothelium-dependent vasodilator brady-kinin induces marked relaxing responses in resis-tance arteries from patients with residual cardio-vascular disease.

• NO-synthase may play a role independent of NO, ONOO- or H2O2

• Bradykinin-induced relaxations were not reduced by indomethacin, L-NAME, ODQ or ebselen in arteries contracted with endothelin-1.

T142

miR-126-5p protects retinal endothelial cells from apoptosis through SetD5 regulation in neurons.

Gaëlle Villain1, Loïc Poissonnier1, Baraa Noueihed2, Gaëlle Bonfils1, Jose Carlos Rivera2, Sylvain Chemtob2, Fabrice Soncin1, Virginie Mattot1

1Univ. Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T – Mechanisms of Tumorigenesis and Target Therapies, Lille, France, 2Department of Pediatrics, Ophthalmology, and Pharmacology, CHU Sainte-Justine Research Center, Université de Montréal, Montréal, Canada

• miR-126-5p is expressed both in retina endothe-lial cells and in retina ganglion cells (RGC).

• During retina vascularisation miR-126-5p pro-tects endothelial cells from apoptosis through the regulation of Sema3A expression in RGC.

• miR-126-5p negatively controls Sema3A expres-sion through the regulation of SetD5

T143

Circulating angiogenic profile reflects tumor vasculature modification under sunitinib in metastatic Renal Cell Carcinoma patients

Laetitia Mauge1,2, Mehdi Bouaboula1,3, Helena Pereira4, Anne-Sophie Gille2, Pr Eric Tartour1,5, Pr Laure Fournier1,3, Pr Stéphane Oudard1,6, Pr Dominique Helley1,2, on behalf of the PREINSUT trial investigators1Université Paris Descartes, UMR-S 970, Paris Cardiovascular Research Center, Paris, France, 2Department of Biological Hematology, Hopital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France, 3Department of Radiology, Hopital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France, 4Unité d’Epidémiologie et de Recherche Clinique, Hopital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, INSERM Centre d’Investigation Clinique 1418, Paris, France, 5Department of Immunology, Hopital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France, 6Department of Medical Oncology, Hopital Européen Georges Pompidou, Assistance Publique-Hôpitaux de Paris, Paris, France

• Blood biomarkers related to angiogenesis can predict the clinical outcome under sunitinib in metastatic renal cell carcinoma (PREINSUT trial).

• Interestingly, VEGF-A/VEGF-R1 ratio evolution under sunitinib inversely correlates with tumor blood volume as measured by perfusion imaging

• Combined VEGF-A related blood biomarkers evo-lution reflects tumor vasculature modification under sunitinib and could be interesting to early detect resistance or relapse to sunitinib.

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T144

Myeloid cell ER-stress response contributes to pathological retinal neovascularization in ischemic proliferative retinopathy

Gaëlle Mawambo1, Malika Oubaha1, Agnieszka Dejda1,2, François Binet2, Przemyslaw Sapieha1,2

1Department of Biochemistry,Maisonneuve-Rosemont Hospital Research Centre, University of Montreal, Montreal, Canada, 2Department of Ophthalmology, Maisonneuve-Rosemont Hospital Research Centre, University of Montreal, Montreal, Canada

• Myeloid cells express the ER-stress effector Inosi-tol-requiring enzyme 1α(IRE1α).

• Inositol-requiring enzyme 1α modulates produc-tion of Vegfa, Il-1β, lL-6 and Tnf-α.

• Myeloid-resident IRE1α influences pathological angiogenesis in ischemic retinopathies.

T145

In-vitro model of the human blood vessel wall

Sandra Mayr1, Boris Buchroithner1,2, Bianca Buchegger2, Jaroslaw Jacak1,2

1University Of Applied Sciences, School of Applied Health and Social Sciences, Linz, Austria, 2Johannes Kepler University, Department of Applied Physics, Linz, Austria

• Multi-photon lithography with biocompatible methacrylates for structuring of three-dimen-sional, mechanical stable scaffolds used in tissue engineering

• In-vitro model of a human blood vessel wall inside a microfluidic seeded with human endo-thelial cells

• Nanoscopy of cells on lithography structures for visualization of biological processes

T146

Skeletal Muscle Cell-Specific Tie2 Signaling Promotes Myoblast Differentiation

Timothy J McCord1, Joseph M McClung2, Brian F Gilmore1, Christopher D Kontos1

1Duke University, Durham, United States, 2East Carolina University, Greenville, United States

• Tie2 and VE-PTP are expressed in regenerating skeletal muscle in vivo and during differentiation in vitro.

• Tie2 signaling and function, regulated in part by the phosphatase VE-PTP, is temporally regulated during skeletal muscle cell differentiation.

• Disruption of Tie2 signaling results in impaired skeletal muscle cell differentiation in vitro and regeneration in vivo.

T147

BMP9 antagonistic effects on the vascular functionality of endothelial colony forming cells

Reinhold Medina1, Christina O’Neill1, Rachel Church1, Joana Melo1, Jasenka Guduric-Fuchs1, Alan Stitt1

1Queen’s University Belfast, Belfast, United Kingdom

• BMP9 promotes endothelial tube formation in ECFCs under basal conditions.

• BMP9 inhibits VEGF-induced ECFC endothelial tube formation.

• BMP9 enhances thrombin-dependent disruption of barrier function in ECFCs; however, it also facil-itates effective recovery.

T148

Inhibition of VEGF-B signaling reduces lip-id-mediated NETosis and improves wound healing in diabetic mice

Annika Mehlem1, Annelie Falkevall1, Jacob Grunler2, Isolde Palombo1, Md Hannes Olausson3, Pierre Scotney4, Andrew Nash4, Md Sergiou Bogdan-Catrina2, Ulf Eriksson1

1Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, , Sweden, 2Department of Molecular Medicine and Surgery, Karolinska Institutet and Karolinska University Hospital, Stockholm, , Sweden, 3Department of Medicine, M54 Karolinska University Hospital, , Sweden, 4CSL Limited, Parkville,, Victoria, , Australia

• Expression of Vascular endothelial factor B and its downstream target fatty acid transport protein 4 are upregulated in skin from diabetic patients and type 2 diabetic mice.

• Wounding of type 2 diabetic mice upregulates the VEGF-B signaling pathway and alter wound lipid composition

• Inhibition of VEGF-B signaling pathway, nor-malizes lipid content, prevents NET release and accelerates wound healing

T149

Improving plaque VSMC phenotype by ener-getic switching.

Craig Docherty1, Andy Carswell1, Miss Rebecca Connor1, Jordan Bresciani1, John Mercer1

1University of Glasgow, Glasgow, United Kingdom

• Energetic switching in plaque VSMC is a new dru-gable target.

• Energetic switching improves VSMC phenotype.• This phenomenon can be targeted to human

plaques.

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T150

Arhgef1 invalidation contributes to blood and vascular wall hypocoagulability independently of arterial stiffness in aged-mice

Nathalie Mercier1, Camille Rouillon1, Gervaise Loirand2, Patrick Lacolley1, Véronique Regnault1

1Université de Lorraine, inserm, DCAC, F-54000 Nancy, France, 2Inserm, UMR 1087, Nantes, France

• Arhgef1 invalidation induced a decreased throm-bin generation in blood and in vascular smooth muscle cells and a decreased platelet activation

• In vivo, the time to thrombus formation was lon-ger in Arhgef1 -/- compared to Arhgef1+/+ mice

• Aged Arhgef1-/- and Arhgef+/+ mice showed a similar arterial stiffness

T151

Functional Regulatory Mechanism of LMOD1 Association with Coronary Artery Disease

Vivek Nanda1, Tina Wang1, Milos Pjanic1, Mr. Boxiang Liu1, Thomas Quertermous1, Joseph Miano3, Nicholas Leeper1, Clint Miller1,2

1Stanford University, Stanford, United States, 2University of Virginia, Charlottesville, United States, 3University of Rochester, Rochester, United States

• Coronary artery disease associated variant rs2820315 is associated with reduced LMOD1 expression in vascular tissues.

• This reduction appears to be mediated through rs34091558 and altered FOXO3 binding to an enhancer in coronary artery smooth muscle cells.

• Changes in vessel wall processes (proliferation, migration, and contraction) through LMOD1 dys-regulation may partially explain the heritable risk for CAD.

T152

Hemodynamic shear stress-regulated Smad signaling in endothelial cells

Elizabeth Min1, Martin Schwartz1

1Yale University, New Haven, United States

• Nuclear retention of R-Smad2/3 peaks at low shear, whereas Smad1 peaks at high (physiologi-cal) shear.

• Shear stress-induced R-Smad1/5/8 activation requires BMP9 or 10, Alk1 and Endoglin.

• In contrast, shear stress-induced R-Smad2/3 acti-vation requires BMP9, Alk5 and Neuropilin1.

T153

Integrated analysis of the mechanical response and mechano-adaptation of endo-thelial monolayers subjected to mechanical strain

Yekaterina Miroshnikova1,2,3,4, Xinping Li1, Sara Wickström1,2,4, Corinne Albiges-Rizo3, Eva Faurobert3

1Max Planck Institute for Biology of Ageing, Cologne, Germany, 2Helsinki Institute of Life Science, Helsinki, Finland, 3Institute for Advanced Biosciences, Grenoble, France, 4Wihuri Research Institute, Helsinki, Finland

• Stretch-activated ion channel-triggered calcium signaling mediates endothelial mechano-re-sponse to exogenously applied strain

• Biphasic waves of Rho and Rac signaling and subsequent remodeling of cell-cell and cell-ECM adhesions are a part of the immediate cellular response to exogenous strain

• Long-term mechano-adaptation to exogenously applied strain is achieved through modifications to the biophysical state of the actin cytoskeleton

T154

Crp3 modulates cellular stiffness and abdomi-nal aortic aneurysm development

Joao C. Ribeiro-Silva1, Ana B. M. Mattos1, Mariana S. A. Ferraz2, Miriam H. Fonseca-Alaniz1, Adriana M. Alencar2, Jose E. Krieger1, Ayumi A. Miyakawa1

1Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil, 2Physics Institute, University of São Paulo, São Paulo, Brazil

• Crp3 is part of the focal adhesion• Crp3 increases SMC stiffness• Absence of Crp3 protects abdominal aortic aneu-

rysm development

T155

Endothelial calpain systems orchestrate myo-fibroblast differentiation during wound healing

Takuro Miyazaki1, Shogo Haraguchi1, Joo-ri Kim-Kaneyama1, Akira Miyazaki1

1Showa University School of Medicine, Tokyo, Japan

• Endothelial cell-driven myofibroblast differentia-tion is responsible for calpain systems in vascular endothelial cells.

• Endothelial calpain systems is required for ensur-ing PDGFR-β in fibroblasts.

• Targeting endothelial calpain systems is sufficient for interfering fibrogenic responses in wound sites and delaying dermal wound healing.

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IVBM2018

T156

Parvins are required for endothelial cell-cell junction organization and proper vasculariza-tion of developing brain

Eloi Montanez Miralles1

1Ludwig-Maximilians-University Munich , Munich, Germany

• α- and β-parvin isoforms have compensatory functions in the endothelium

• Mice with ECs lacking parvins display hemor-rhages, reduced vessel branching and severe vas-cular defects in CNS including balloon-like hemor-rhagic endothelial clusters

• Parvins are required for proper VE-cadherin local-ization at cell-cell junctions and endothelial api-cal-basal polarity

T157

In vivo visualization of hepatic lipid droplets accumulation and microenvironment in nonal-coholic steatohepatitis mouse model

Jieun Moon1, Yoonha Hwang1, Eunjoo Song1, Pilhan Kim1

1Korea Advanced Institute of Science and Technology, Daejeon, South Korea

• Nonalcoholic steatohepatitis (NASH) is the rapidly increasing chronic liver disease worldwide.

• To understand cellular-level pathogenesis of NASH, a repetitive longitudinal visualization of hepatic microenvironment in NASH model is highly desirable.

• We visualized lipid droplet deposition and hepatic microenvironment of NASH model in vivo by using custom-built real-time confocal microscopy.

T158

Cell type specific expression of Coronary Artery Disease genes

Pierre Moreau1, Maria Bouvy-liivrand2, Associate Minna Kaikkonen-Määttä1

1A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland, 2School of Medicine, University of Eastern Finland, , Finland

• According to genome-wide analysis, endothe-lial cells, smooth muscle cells and macrophages exhibit highly cell-type specific responses to proatherogenic stimuli.

• Each cell type response affects different sets of genes that have a significant effect on genes within distinct molecular and cellular pathway.

• Interaction between cell type specific and stim-uli specific transcription factors are most likely responsible for those differences.

T159

Correlating clinical risk factors and histo-logical features in ruptured and unruptured human intracranial aneurysms

Sandrine Morel1,2, Mannekomba Diagbouga1, Nicolas Dupuy1,2, Esther Sutter1, Vincent Braunersreuther3, Graziano Pelli1, Marco Corniola2, Renato Gondar2, Max Jägersberg2, Nathalie Isidor2,4, Karl Schaller2, Marie-Luce Bochaton-Piallat1, Philippe Bijlenga2, Brenda Kwak1,5

1Department of Pathology and Immunology, University of Geneva, Geneva, Switzerland, 2Neurosurgery Division, Department of Clinical Neurosciences, Geneva University Hospitals, Geneva, Switzerland, 3Department of Clinical Pathology, University of Geneva and Geneva University Hospitals, Geneva, Switzerland, 4Clinical Trial Unit, Geneva University Hospitals, Geneva, Switzerland, 5Department of Medical Specializations – Cardiology, University of Geneva, Geneva, Switzerland

• Intracranial aneurysm walls prone to rupture present a lower content in smooth muscle cells and collagen, and a higher content in macro-phages.

• Collagen content is affected by the thickness of the aneurysmal wall in unruptured intracranial aneurysms.

• Intracranial aneurysms undergo structural alter-ations relatively well associated with clinical and radiological factors used to predict the risk of rupture.

T160

uPARAP/endo180 : a new player in lymph-edema physiopathology

Florent Morfoisse1, Giulia Vottero2, Sylvia Blacher1, Maureen Van de Welde1, Marie Ebroin1, Isabelle Bourgot1, Jean-luc Nizet2, Agnes Noel1

1University of Liege-GIGA Center-LBTD, Liege, Belgium, 2University Hospital Liege-Department of Plastic Surgery, Liege, Belgique

• uPARAP/endo180 is implicated in lymphedema development.

• uPARAP genetic ablation decreases edema sever-ity in a hind limb model

• uPARAP acts on lymphatic microenvironment by modulating inflammatory cytokines expression level.

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IVBM2018

T161

Reduced proliferation in pancreatic cancer with VEGF receptor-2/Neuropilin-1 complex formation in trans

Eric Morin1, Elin Sjöberg1, Vegard Tjomsland2, Chiara Testini1, Sara Kiflemariam1, Tobias Sjöblom1, Lena Claesson-Welsh1

1Uppsala University, Dept Immunology, Genetic and Pathology, Uppsala, Sverige, 2University of Oslo, Department of Hepato-pancreato-biliary Surgery, Oslo, Norway

• VEGFR2 and Neuropilin-1 can form complexes between endothelial cells and tumor cells (trans).

• Trans complexes can be visualized in human patient material by in situ proximity ligation assay.

• Trans complexes are correlated with reduced vessel area, vessel branching and tumor cell pro-liferation in pancreatic ductal adenocarcinoma patients.

T162

The extracellular environment supporting lym-phatic vessels and valves

Nanami Morooka1,2, Naoki Mochizuki2, Kiyotoshi Sekiguchi1

1Institute for Protein Research, Osaka University, Suita, Japan, 2National Cerebral and Cardiovascular Center Research Institute, Suita, Japan

• Lymphatic endothelial cells in lymphatic trunk and those in luminal valves are supported by dif-ferent integrin-extracellular matrix complex

• Laminin 411 (alpha4beta1gamma1) and/or lami-nin 421 (alpha4beta2gamma1) associate with lymphatic endothelial cells in collecting lymphatic trunk

• Laminin 521 (alpha5beta2gamma1) is mainly used as a substrate for endothelial cells in lym-phatic valve leaflets

T163

Endothelial HLA-A2 activation increases neu-trophil transmigration in an in vitro two-hit model

Sofia Morsing1, Claudia Al-Mardini2, Leendert Porcelijn1, Alexander Vlaar3, Jaap van Buul1

1Sanquin, Amsterdam, Netherlands, 2University of Amsterdam, Amsterdam, Netherlands, 3Academic Medical Center, Amsterdam, Netherlands

• Cognate antibodies to Human Leukocyte Antigen A2 (HLA-A2) in transfused blood products are commonly found after patients developed anti-body-mediated Transfusion-Related Acute Lung Injury (TRALI)

• Endothelial HLA-A2 binding results in increased cell-cell junction disruption in combination with lipopolysaccharide stimulation

• Endothelial HLA-A2 binding increases transen-dothelial migration of neutrophils under physio-logical flow, unrelated to increases in endothelial inflammatory markers

T164

Pre-clinical development and testing of Maga-cizumab, a therapeutic antibody against LRG1

Stephen Moss1, David Kallenberg1, Vineeta Tripathi1, Sterenn Davis1, Jestin George1, Dr Marie O’Connor1, Laura Dowsett1, John Greenwood1

1UCL Institute Of Ophthalmology, London, United Kingdom

• LRG1 contributes to pathological angiogenesis• Magacizumab is a function-blocking humanised

antibody that inhibits LRG1• LRG1 blockade leads to vessel normalisation and

inhibition of angiogenesis in mouse models of retinal vascular disease and cancer

Posters – Tuesday

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IVBM2018

T165

PTEN regulates the inflammatory dedifferen-tiated phenotype of smooth muscle cells and the severity of atherosclerosis

Karen Moulton1, Sizhou Lu2, Rebecca Tucker2, Marcella Li1, Marie Mutryn2, Mary Weiser-Evans2

1Division of Cardiology, Dept. of Medicine, University of Colorado Anschutz Medical Campus, Aurora, United States, 2Division of Renal Diseases and Hypertension, Dept. of Medicine, University of Colorado Anschutz Medical Campus, Aurora, United States

• Loss of PTEN in smooth muscle cells (SMCs) pro-motes SMC dedifferentiation and a pro-inflam-matory phenotype.

• Loss of PTEN in SMCs promotes atherosclerosis.• Systemic over-expression of PTEN inhibits the

development of atherosclerosis.

T166

Altered angiogenesis in Duchenne muscular dystrophy mice: the role of heme oxygenase-1

Olga Mucha1, Paulina Podkalicka1, Mateusz Tomczyk1, Kinga Rusin1, Iwona Bronisz-Budzynska1, Magdalena Kozakowska1, Witold Nowak1, Alicja Jozkowicz1, Jozef Dulak1, Agnieszka Loboda1

1Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland

• It is suggested that angiogenesis process might be altered in Duchenne muscular dystrophy dis-ease.

• We showed that several angiogenesis-related genes and proteins are changed in dystrophic mice in comparison to wild type counterparts.

• Additionally, lack of heme oxygenase-1 impairs neovascularization in mice after hindlimb isch-emia, suggesting its contribution to this process.

T167

The scaffolding protein Caskin2 regulates vas-cular homeostasis downstream of Angiopoie-tin/Tie receptor signaling

Sarah Mueller1, Timothy McCord1, Michael Padgett1, Jianhua Huang1, Shubhangi Arora1, Christopher Kontos1

1Duke University, Durham, United States

• Caskin2 is a previously uncharacterized scaffold-ing protein that interacts with Tie1 and negatively regulates Tie1 expression.

• Caskin2 promotes phosphorylation of eNOS on the activating residue S1177 and is required for Ang-1/Tie2-mediated activation of Akt.

• Loss of Caskin2 in vivo promotes angiogenesis while Caskin2 overexpression in vitro promotes endothelial cell quiescence.

T168

Single-cell RNA transcriptome analysis of perivascular cells

Lars Muhl1, Guillem Genové1, Stefanos Leptidis1, Jianping Liu1, Liqun He2, Giuseppe Mocci1, Åsa Segerstolpe1, Sonja Gustafsson1, Xidan Li1, Michael Vanlandewijck1,3, Emil Hansson1, Christer Betsholtz1,3

1Karolinska Institutet / Integrated Cardio Metabolic Centre (ICMC), Huddinge, Sweden, 2Tianjin Medical University General Hospital Neurological Institute / Key Laboratory of Post-Neuroinjury Neuro-Repair and Regeneration in Central Nervous System, Tianjin, China, 3Uppsala University / Department of Immunology, Genetics and Pathology, Uppsala, Sweden

• scRNA-seq is an unprecedented method to iden-tify and characterize rare or subtle cell types,

• Perivascular cells can be classified by their molec-ular fingerprints into pericytes, vascular smooth muscle cells, fibroblast-like cells and further sub-classes of these three cell-archetypes,

• Perivascular cells exhibit an organotypic pheno-type.

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IVBM2018

T169

Neuropilin-1 maintains dimethylarginine dimethylaminohydrolase 1 expression in endothelial cells and regulates angiotensin II induced-hypertension

Debabrata (Dev) Mukhopadhyay1

1Mayo Clinic College Of Medicine And Science , Jacksonville, United States

• Neuropilin-1 (NRP1) regulates Dimethylarginine dimethylaminohydrolase-1 (DDAH-1), which is known to degrade asymmetric dimethylarginine (ADMA), an endogenous inhibitor of endothelial nitric oxide synthase (eNOS) in vascular endothe-lial cells.

• The regulation of NRP1 on DDAH1 expression is mediated by a post-transcriptional mechanism involving miR-219-5p.

• NRP1 controls DDAH1 expression and contrib-utes to blood pressure regulation under stress of angiotensin II infusion.

T170

The Role of the PECAM/VE-Cadherin/VEGFR2 Mechanosensing Complex in Initiating Tran-sendothelial Migration.

Evan Weber1, David Sullivan1, Tao Fu1, Natalya Diaz1, William Muller1

1Northwestern University Feinberg School Of Medicine, Chicago, United States

• LeukocytePECAM-mediatedclusteringofendo-thelial cell PECAM activates TRPC6 to trigger↑[Ca2+]i required for transendothelial migra-tion(TEM).

• PECAM clustering on endothelial cells activatesVEGFR2,whichactivatesPLCγ1,whichproducesdiacylglyceroltoactivateTRPC6.

• We hypothesize a novel role for the endothelial cell PECAM/VE-cadherin/VEGFR2 mechanosen-sory complex in translating mechanical signals not involving fluid shear.

T170

Fetuin-A and adiponectin levels in type 2 dia-betic and obese post menopausal women

Sara Paccosi1, Laura Pala2, Barbara Cresci2, Carlo,Maria Rotella2,3, Astrid Parenti1

1Dept. of Health Sciences; University of Florence, Florence, Italy, 2Diabetology, Careggi University Hospital, Florence, Italy, 3Dept. of Biomedical Clinical and Experimental Sciences, Endocrine Unit, University of Florence, Florence, Italy

• Fetuin-A plasma levels increase in type 2 diabetes (T2D) or obese patients but its pathogenetic role is still unclear.

• Is there any correlation between fetuin-A and adiponectin plasma levels in obese and/or T2D post-menopausal women?

• Our results show changes in fetuin-A and adi-ponectin levels related to body weight in post-menopausal women with cardiovascular risk.

T171

Enhancing the efficacy of immunotherapy of NSCLC using new RGD-mimetic prodrug

Jose Manuel Muñoz Félix1, Juliana Candido2, Michael Weinmüller3, Hosrt Kessler3, Kairbaan M Hodivala-Dilke1

1Centre for Tumour Biology, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square, London. , London, United Kingdom, 2Centre for Cancer and Inflammation, Barts Cancer Institute - a CR-UK Centre of Excellence, Queen Mary University of London, John Vane Science Centre, Charterhouse Square., London, United Kingdom, 3Institute for Advanced Study and Center for Integrated Protein Science, Department of Chemistry, Technische Universität München, Lichtenbergstr. , Garching, Germany

• Agent X is a new orally available RGD-mimetic that promotes tumour angiogenesis without affecting tumour growth.

• Agent X reduces tumour growth when is adminis-tered in combination with cisplatin and promotes an immunopermissive tumour microenviron-ment.

• Our data provide evidence that the oral adminis-tration of agent X /cisplatin and immunotherapy is an effective strategy for lung cancer control

Posters – Tuesday

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IVBM2018

T172

In vivo imaging analysis of combined chemo-therapy resistant glioblastoma multiforme

Fumitaka Muramatsu1, Hiroyasu Kidoya1, Yohei Tsukada1, Yumiko Hayashi1, Tomohiro Iba1, Hisamaichi Naito1, Nobuyuki Takakura1

1Osaka University, 3-1, Yamadaoka, Suita City, Japan

• Construction of the tumor angiogenesis in vivo imaging system

• Anti-angiogeneic therapy resistant endothelial cells remain in the tumor as well perfused ves-sels.

• Blood vessel and tumor cell positional relation-ships under combined chemotherapy

T173

Inhibition of SDF-1α/CXCR4 signaling abro-gates the blood-retina barrier disruption induced by pericyte-deficiency

Keisuke Omori1, Kaori Kurata2, Yoko Fukushima3, Nobutaka Fujii4, Tomoko Namba-Hamano5, Yoshitsugu Takabatake5, Marcus Fruttiger6, Takashi Nagasawa7, Akiyoshi Uemura2, Takahisa Murata1

1Department of Animal Radiology, The University of Tokyo., Tokyo, Japan, 2Department of Retinal Vascular Biology, Nagoya City University., Nagoya, Japan, 3Department of Ophthalmology, Osaka University., Oasaka, Japan, 4Laboratory of Bioorganic Medicinal Chemistry and Chemogenomics, Kyoto University., Kyoto, Japan, 5Department of Nephrology, Osaka University., Osaka, Japan, 6UCL Institute of Ophthalmology, University College London., London, United Kingdom, 7Department of Immunobiology and Hematology, Kyoto University., Kyoto, Japan

• Pericyte deficiency disrupted the blood-retina barrier and cause edema in mouse retina.

• The expression of stromal derived factor-1α was elevated in retinal endothelial cells after pericyte deficiency.

• Pharmacological blockade of CXCR4 or EC-specific gene disruption of CXCR4 restored the disruption of blood-retina barrier.

T174

Identification and characterization of VEGF-A enhancers

Isidore Mushimiyimana1, Nihay Laham-Karam1, Henri Niskanen1, Associate Minna Kaikkonen-Määttä1, Seppo Ylä-Herttuala1

1Molecular Medicine Group, A.I. Virtanen Institute, University of Eastern Finland, Kuopio FI-70210, Finland

• Using both HUVECs ChIP-seq and Hi-C data, we identified six putative enhancers interacting with the VEGF-A promoter.

• We identified two enhancers that induced reporter gene expression although their differen-tial activation was also noticed under hypoxia and normoxia.

• The present study revealed VEGF-A regulatory enhancers that could be potential therapeutic targets for endogenous regulation of VEGF-A expression.

T175

Coordinated regulation of endothelial calcium signalling and flow-induced nitric oxide pro-duction by PKC-beta and PKC-eta

Tenderano Muzorewa1, Dov Jaron1, Donald Buerk1, Kenneth Barbee1

1Drexel University, Philadelphia, United States

• PKC-beta and PKC-eta differentially regulate flow-induced NO production by modulating eNOS activity and calcium entry respectively

• PKC-eta regulation of flow-induced NO produc-tion is essential and is achieved through regula-tion of store-operated calcium entry in BAECs

• On the background of ubiquitous endothelial calcium signaling, calcium-dependent PKCβ and calcium-independent PKCη tightly regulate endo-thelial response to flow

Posters – Tuesday

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IVBM2018

T176

Homocysteine alters von Willebrand factor activity by modulating the size of Weibel-Pal-ade bodies.

Francesca Patella1, Dominic Scaglioni1, Daniel Cutler1

1UCL, , United Kingdom

• Homocysteine levels control Weibel-Palade body length and thus VWF functioning.

• Pathophysiological concentrations of homocys-teine lengthen Weibel-Palade bodies, increasing endothelial pro-haemostatic activity.

• Vitamins B12 and Folate counteract the effects of homocysteine on Weibel-Palade bodies and Von Willebrand Factor.

T177

PDGFRalpha regulates pulmonary PW1+ pro-genitor cells recruitment during early chronic hypoxia-induced vessel neomuscularization

Lamiaa El Bernoussi1, Jessica Raimbault-Machado1, Nilay Akkoyunlu1, France Dierick1, Bénédicte Hoareau-Coudert2, Catherine Pavoine1, Giovanna Marazzi1, David Sassoon1, Pr Florent Soubrier1, Sophie Nadaud1

1Inserm U1166, Paris, France, 2CYPS Plateform, Paris, France

• CD34+/PW1+/PDGFRα+ pulmonary progenitor cells are recruited and participate in vascular remodeling during chronic hypoxia (CH), a pul-monary hypertension mouse model.

• Inhibition of the PDGFR pathway prevents pro-genitor cells proliferation, differentiation and participation in vascular neomuscularization whereas activation of PDGFRα promotes neo-muscularization

• These results suggest that PDGFRα is an import-ant regulator of progenitor cells’ function

T178

Inhibition of Notch signaling in pericytes results in arteriovenous malformations

Taliha Nadeem1, Jonathan Cothran1, Henar Cuervo1

1University Of Illinois At Chicago, Chicago, United States

• Pericyte-specific Notch signaling is ablated by crossing PDGFRβ-P2A-CreERT2 mice with Rbpj-flox/flox mice.

• Absence of pericyte Notch signaling results in arteriovenous malformations.

• Mice with loss of perivascular Notch exhibit irreg-ular smooth muscle cell distribution, and a signif-icant reduction in pericyte coverage.

Posters – Tuesday

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IVBM2018

T179

The role of endothelium-derived PDGF-B as a survival factor for pericytes in adult mouse brain

Khayrun Nahar1, Maarja Andaloussi-Mäe1, Giacomo Bertuzzi1, Annika Keller2, Christer Betsholtz1

1Uppsala University, Dept. Of Immunology, Genetics and Pathology, Division of Vascular Biology Dag Hammarskjölds väg 20, Uppsala, Sweden, 2Department of Neurosurgery University Hospital Zürich, Zürich University Frauenklinikstrasse 10, Zürich, Switzerland

• Endothelial-derived PDGF-B is required for peri-cyte investment to vessel wall during develop-ment

• Whether the ablation of PDGF-B in adult micehaveanyeffectsonthevasculatureandpericytesurvivalinmurinebrainisstillunknown

• ConditionalknockoutapproachinadultmicetodeletePdgfbspecificallyinECwasusedtoinvesti-gatetheeffectsonpericytesurvival

T180

Ligand-specific Notch decoys as potential anti-angiogenic biotherapeutics

ReyhaanChaudhri2, Mr. James Herts1,Mr.TimothySargis1, L. A. Naiche1,JanKitajewski1

1University Of Illinois Chicago, Chicago, United States, 2NuVasive, San Diego, United States

• Notch decoys are potential biotherapeutic pro-teinsthatcanspecificallytargetJagged-orDll-in-duced Notch signaling

• Inhibition of Jagged signaling may block tumorgrowthandmetastasis

• A novel Jagged-specific Notch decoy showspotential as a therapeutic for triple negativebreastcancer

T181

CD157 marks tissue resident vasculorepara-tive endothelial stem cells

Hisamichi Naito1,TakuWakabayashi1,TomohiroIba1, NobuyukiTakakura1

1Osaka University, Japan

• CD157 marks adult resident vascular endothelial stem cells in mouse.

• OnesingleCD157+endothelialcellcanreconsti-tutesbloodvesselintheliver.

• Geneticlineagetracingrevealsahierarchicalvas-cularendothelialcellsysteminthelivervascula-ture.

T182

Transcriptional regulation and physiological significance of novel BMP-ALK1 signal target genes in vascular endothelial cells

YumiKatayama-Kinugasa1,YukihiroHarada1,2, Toru Tanaka1,KoichiNishiyama3,TeruhisaKawamura2,YusukeWatanabe1, Osamu Nakagawa1

1Department of Molecular Physiology, National Cerebral and Cardiovascular Center Research Institute, Suita,, Japan, 2Department of Biomedical Sciences, Ritsumeikan University College of Life Sciences, Kusatsu,, Japan, 3International Research Center for Medical Sciences, Kumamoto University, , Japan

• We identified novel target genes of BMP-ALK1signaling in vascular endothelial cells, SGK1 and TMEM100.

• Deletionofthesegenescausedseveredefectsofvascularmorphogenesisandembryonic lethalityin mice.

• Both genes are specifically expressed in endo-thelialcellsduringmouseembryodevelopment,whilethemodeoftheirtranscriptionalregulationissignificantlydifferent.

T183

Significance of the Hey family of transcription factors during cardiovascular development

DrYusukeWatanabe1,2, Mr Shuhei Ishii1,2, Mr Taiki Uemoto1,2, Dr Tomoe Nakamura-Nishitani1, Dr Daiki Seya1, Mr Dai Ihara1,3,DrTeruhisaKawamura3, Dr Osamu Nakagawa1,2

1National Cerebral and Cardiovascular Center, Suita,, Japan, 2Nara Medical University Graduate School of Medical Sciences, Kashihara,, Japan, 3Department of Biomedical Sciences, Ritsumeikan University College of Life Sciences, Kusatsu,, Japan

• Heytranscriptionfactorsaredownstreammedia-torsofNotchandBMP-ALK1signaling.

• Theirembryonicexpressioniscontrolledthroughacombinationofdistalenhancers.

• Severe phenotypes in their knockoutmice indi-cateuniqueaswellasoverlappingrolesessentialfor cardiovascular development.

Posters – Tuesday

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IVBM2018

T184

A novel type of flow-dependent angiogenesis in zebrafish

Hiroyuki Nakajima1, Naoki Mochizuki1,2

1Department of Cell Biology, National Cerebral And Cardiovascular Center Research Institute, Suita, Japan, 2AMED-CREST, National Cerebral And Cardiovascular Center Research Institute, Suita, Japan

• Wecharacterizedanovelflow-dependentangio-genesisprocessintheaorticarch(AA)ofzebraf-ish

• The flow-dependent bud-shaped protrusivesprout started from invagination of endothelialsheetsmaintainingapico-basalpolarity

• Intracellular Ca2+ oscillations occurred inresponse to blood flow specifically in the bud-shaped endothelial cells.

T185

The role of Gs-mediated signaling in endothe-lial inflammation

Akiko Nakayama1,StefanOffermanns1,LeeWeinstein2

1Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany, 2National Institutes of Health, Bethesda, USA

• Mice lacking endothelial G-protein alpha s (Gαs) showedincreasedatheroscleroticlesionandele-vated endothelial expression of monocyte che-motacticprotein1.

• Knock-down of Gαs in endothelial cells (ECs) resulted in up-regulated nuclear factor-κB phos-phorylationunderbasalandafteroscillatoryflowexposure.

• Several candidates of G-protein-coupled recep-tors (GPCRs) operating upstream in ECs havebeen identified, and their in vivo functions arecurrentlyanalyzed.

T186

Semaphorin 3F inhibits breast tumor angio-genesis and metastasis via Akt-mTOR path-way

Hironao Nakayama1,2,3,AyumiNakazawa1, Natsuki Sawatari1, Akari Murakami4,HisayoNishida-Fukuda4, YoshiakiKamei4,YasutsuguTakada4,ShigekiHigashiyama2,3

1Department of Medical Science and Technology, Hiroshima International University, Higashi-hiroshima, Japan, 2Division of Cell Growth and Tumor Regulation, Proteo-Science Center, Ehime University, Toon, Japan, 3Department of Biochemistry and Molecular Genetics, Ehime University Graduate School of Medicine, Toon, Japan, 4Department of Surgery, Hepato-biliary-pancreatic Surgery and Breast Surgery, Ehime University Graduate School of Medicine, Toon, Japan

• SEMA3F inhibits Akt-mTOR signaling pathway inhumanbreasttumorcells.

• Statistical analysis indicated a close associationbetween reduced expression of SEMA3F withthatofpoorpatient’ssurvival.

• SEMA3Fisapromisinginhibitorofbreasttumorgrowth,angiogenesisandmetastasis.

T187

Tumor microenvironment-dependent endo-thelial cell heterogeneity is regulated by matri-cellular protein SPARCL1 in human colorectal carcinoma

Elisabeth Naschberger1,DanielaRegensburger1, Clara Tenkerian1, Anika Klingler1, Nathalie Britzen-Laurent1, Valerie S Meniel3, Susanne Merkel2, Vera S Schellerer2, Michael Stürzl1

1Division of Molecular and Experimental Surgery, University Medical Center Erlangen, Erlangen, Germany, 2Department of Surgery, University Medical Center Erlangen, Erlangen, Germany, 3European Cancer Stem Cell Research Institute, Cardiff University, Cardiff, United Kingdom

• CellularmemoryofcultivatedTECsreflectstumormicroenvironment (TME)

• SPARCL1 indicates TME-dependent heterogene-ityofTECsandregulatesbloodvesselquiescenceandmaturationincolorectalcancer

• SPARCL1isaTEC-derivedhomeostasisfactorcon-tributingtotheanti-tumor-defense

Posters – Tuesday

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IVBM2018

T188

Vein Identity Requires BMP Signalling Through ALK3

Alice Neal1, Svanhild Nornes1,SophiePayne1,MartinFritzsche1,MarshaD.Wallace1,RobertN.Wilkinson2, Kira M. Chouliaras1, Ke Liu3,KarenPlant2, Radhika Sholapurkar1, WiebkeHerzog4, Gareth Bond1, Tim Chico2, George Bou-Gharios3, Sarah De Val1

1The University of Oxford, Oxford, United Kingdom, 2University of Sheffield, Sheffield, United Kingdom, 3University of Liverpool, Liverpool, United Kingdom, 4University of Muenster, Muenster, Germany

• PerturbationstoBMPsignallinginbothmiceandzebrafish result in aberrantearly vein formationandidentitybutdonotaffectearlyarterialdevel-opment.

• BMPsignallingactivatesvenousdifferentiationviatheALK3(BMPR1A)receptorandSMAD1/SMAD5bindingatenhancersofveinspecificgenes.

• The specificity of SMAD1/SMAD5-mediatedvenous gene activation is unaffected by Notchinhibition.

T189

Lethal irradiation abolishes smooth muscle cell investment into BCA and carotid artery lesions

Alexandra Newman1,RichardBaylis1, Daniel Hess1, Laura Shankman1,StevenGriffith1, Olga Cherepanova1,GaryOwens1

1University Of Virginia, Charlottesville, United States

• Radiationexposure increases cardiovasculardis-ease incidence and atherosclerosis development

• Lethal irradiation inhibits investment of smoothmuscle cells into atherosclerotic lesions in thebrachiocephalicarteryorvascularinjury-inducedcarotidneointima

• Lethalirradiationselectivelyimpactsneural-crestderived SMC; lesions in various other vascularbedsdidnotshowlossofSMCinvestment

T190

VEGF-B gene therapy decreases macrophage uptake of modified LDL, foam cell formation, and atherosclerosis

Su D. Nguyen1,MariusR.Robciuc1,2, Maija Ruuth1, Harri J. Nurmi1,2, Shou Chen2, Jenni Huusko3, Eero Mervala4, Seppo Ylä-Herttuala3,5,6, Katariina Öörni1, Kari Alitalo1,2

1Wihuri Research Institute, Helsinki, Finland, 2Translational Cancer Biology Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland, 3A. I. Virtanen Institute for Molecular Sciences, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland, 4Department of Pharmacology, Faculty of Medicine, University of Helsinki, Helsinki, Finland, 5Gene Therapy Unit, Kuopio University Hospital , Kuopio, Finland, 6Heart Center, Kuopio University Hospital, Kuopio, Finland

• VEGF-Breducedthemonocyte/macrophagecon-tentinatheroscleroticlesions,andtheuptakeofacetylated LDL and foam cell formation in cul-tured macrophages

• VEGF-B suppressed the expression of scavengerreceptors(SR-AI,CD36orLOX-1)butdidnotaltertheexpressionofABCA1,ABCG1orSR-BI

• VEGF-B protects against atherosclerosis develop-mentwithoutchangesinplasmalipidlevels

T191

Image correlation methods to map blood flow velocities in complex vessel networks

Laura Sironi1,MargauxBouzin1, Donato Inverso2, Nicolò Ceffa1,FabrizioRadaelli1, Laura D’Alfonso1,PabloBlinder3, Maddalena Collini1, Giuseppe Chirico1

1Physics Department, Università degli Studi di Milano-Bicocca, Milano, Italy, 2German Cancer Research Center Division of Vascular Oncology and Metastasis , Heidelberg, Germany, 3Neurobiology Dept., Wise Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv, Israel

• Differentsetups,basedonconfocal/multi-photonscanning systems, and on advanced structuredilluminationmodalities(single-planeillumination,multi-spotmicroscopy)havebeenimplemented.

• The blood flow velocity is extracted from theimagesby spatiotemporal image (cross)-correla-tionspectroscopy.

• The blood flow velocity is monitored both inzebrafish embryos and in the intricate murinehepatic and brain microcirculatory system,together with relevant morphological parame-ters.

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IVBM2018

T192

microRNA-dependent regulation of biome-chanical genes establish tissue stiffness homeostasis

Dr Stefania Nicoli1

1Yale University , New Haven, United States

• RNAmetabolismofstructuralgenes ispreferen-tiallycontrolledbymiRNAs.

• miRNAs mediated the mechanotransduction ofcellsadaptingtostiffsubstrates.

• Stiffnesshomeostasisdrivestissueregeneration

T193

Exploring the vascular link between metabolic dysfunction and stroke

Ingrid Nilsson1, Enming Su2, Linda Fredriksson1,2,ChristineMössinger1,ChristinaStefanitsch1, Lars Muhl1, Anna Olverling1,Anna-LisaLawrence2, Manuel Zeitelhofer1, Milena Z. Adzemovic1, Tofan Taeri1, Erik Samén3, Li Lu3, Sharon Stone-Elander3, Annika Mehlem1, Annelie Falkevall1, Richard F. Keep4,DanielA.Lawrence2, Ulf Eriksson1

1Department of Medical Biochemistry and Biophysics, Division of Vascular Biology, Karolinska Institute, Stockholm, Sweden, 2Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor, USA, 3Karolinska Experimental Research and Imaging Center, Karolinska University Hospital, Stockholm, Sweden, 4Department of Neurosurgery, University of Michigan, Ann Arbor, USA

• Vascular endothelial growth factor–B regulatedreprogramming of endothelial nutrient transport impactsBBBcontrolandoutcomeafterischemicstroke.

• VEGF-B targeting prevented ectopic cerebrovas-cular lipid uptake after stroke correlating withimprovedbrainglucoseuptakeandmetabolism.

• AmelioratingcerebrovascularlipidintoxicationbyVEGF-Binhibitionshowspromiseasanovelcan-didate for future treatment for stroke.

T194

Characterizing the role of VEGF-B in pancre-atic islet lipid handling and beta-cell function

Frank Chenfei Ning1

1Karolinska Institutet, Stockholm, Sweden

• VEGF-B selective deletion in beta-cell does notaffectglucosehomeostasisundernormaldiet

• UnderHFD,VEGF-Bselectivedeletioninbeta-cellcause altered glucose homeostasis

• VEGF-B selective deletion increase islet insulingeneexpression,insulincontentandsecretion

T195

A reconstitution assay system for understand-ing angiogenic morphogenesis: the morpho-genetic function of perivascular pericytes

MichieUchikawa1, Koichi Nishiyama1, Chiharu Esumi1, AkiyoshiUemura2, Sanshiro Hanada1,YuichiroArima1,YujiNashimoto3, Akiko Nakamasu1,RyujiYokokawa3, Takashi Miura4

1Kumamoto University, Kumamoto , Japan, 2Nagoya City University, Nagoya, Japan, 3Kyoto University, Kyoto, Japan, 4Kyushu University, Fukuoka, Japan

• Weestablishedaculturemethodformurinepri-mary endothelial cells and pericytes, which areusefulforfunctionalangiogenesisassays.

• Wedevelopedanexvivoassay,whichenablesusto assess roles of individual cellular components in angiogenic morphogenesis.

• Using the reconstitutionassay,we showedperi-cytestoenhanceangiogenicbranchformation.

T196

Endothelial cell differentiation is encom-passed by changes in long range interactions between inactive chromatin regions

Henri Niskanen1,IrinaTuszynska2,RafalZaborowski2, Merja Heinäniemi3,SeppoYlä-Herttuala1,4, Bartek Wilczynski2, Minna Kaikkonen1

1A.I.Virtanen Institute for Molecular Sciences, University Of Eastern Finland, Kuopio, Finland, 2Institute of Informatics, University of Warsaw, Warsaw, Poland, 3Institute of Biomedicine, University Of Eastern Finland, Kuopio, Finland, 4Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• EC-differentiation involves establishment ofEC-specific units of chromosome organization,which associate with super-enhancers, EC-spe-cific transcription, histone modifications andbindingoftranscriptionfactorsandcohesin

• EC-specific long-range interactions betweentopologically-associating domains are formedwhenheterochromatin is establishedduring lin-eage-specification

• Hypoxia doesn’t alter EC genome organizationand HIF1-alpha utilizes pre-determined chro-matin interactions to drive gene expression inhypoxicconditions

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T197

Restricted S1P signalling at the blood-brain barrier

Anja Nitzsche1,MarinePoittevin1,2,PhilippeBonnin2,3, AmmarBenarab1,SylvainGalvani4,PatriceTherond5, Thomas Mathivet1, Mari Kono6,LudovicCouty1, Richard L . Proia6,NathalieKubis2,3,TimothyHla4, Eric Camerer1

1INSERM U970, Paris Cardiovascular Research Center, Paris, France, 2INSERM U965, Hôptial Lariboisière, Paris, France, 3AP-HP, Hôpital Lariboisière, Physiologie Clinique – Explorations-Fonctionelles, Paris, France, 4Vascular Biology Program, Boston Children’s Hospital, Department of Surgery, Harvard Medical School, Boston, USA, 5AP-HP, Hôpital Bicêtre, Service de Biochimie, Le Kremlin Bicêtre, France, 6Genetics of Development and Disease Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, USA

• ProtectiveroleofS1Preceptor-1incerebralisch-emia

• LocalS1Psourcesmediatereceptoractivationinthiscontext

• S1P1 signalling reporter mice reveal restrictedligandexposureattheblood-brainbarrier

T198

uPARAP/endo180: a novel partner of VEG-FR-2/R-3 that controls VEGF-C-induced lym-phatic sprouting

Agnes Noel1, Tania Durré1,CharlotteErpicum1, Florent Morfoisse1,MarieEbroin1,PhDSilviaBlacher1, Christophe Deroanne2, Thomas Louis1, Seppo Kaijalainen3, Lars Engelholm4, Kari Alitalo3, Niels Behrendt4,JennyPaupert1

1University of Liege, Laboratory of Tumor and Development Biology, GIGA-Cancer, Belgium, 2University of Liege, Laboratory of Connective Tissues Biology, GIGA-Cancer, Belgium, 3University of Helsinki, Wihuri Research Institute and Translational Cancer Biology Program, Biomedicum Helsinki, Finland, 4University of Copenhagen, The Finsen Laboratory/BRIC, Rigshospitalet, Denmark

• uPARAP/endo180isanovelactorofpathologicallymphangiogenesis,butnotangiogenesis.

• uPARAP/endo180 restricts VEGFR2/VEGFR3 het-erodimerisation under VEGF-C stimulation andpromotes VEGFR-3 signaling through Crk-II/JNK/paxillin/Rac1pathway.

• Ourworkhighlightsnovelmolecular featuresofVEGFR-2/VEGFR-3crosstalkthatinvolvesuPARAP/endo180whosefunctioninvascularbiologywasnotknown.

T199

Sox17 regulates blood-brain barrier integrity in hypertensive conditions

Tae Wook Noh1,SooHyunKim1,ChanSoonPark1, Jee MyungYang1, Injune Kim1

1Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea

• Endothelial-specific Sox17 deletion induceshyper-permeability of adult brain vessels inangiotensin(ATII)-infusedcondition.

• ATII-inducedbarrierdisruptioninSox17-deficientadultbrainvessels is characterizedby increasedvesicularactivityandlooseningoftightjunctionsin endothelial cells.

• Sox17mayprotectbarrier integrityofbrainves-selsfromhypertensivestresses.

T200

Thymosin beta 4 Promotes Migration, Endo-thelial Differentiation and Angiogenesis in Human Adipose-Derived Stem Cells

Ji-Min Noh1, Jong-Ho Kim1, I-Rang Lim1,HyungJoonJoo1, Seung-Cheol Choi1, Soon Jun Hong1, Do-sun Lim1

1Department of Cardiology, Cardiovascular Center, College of Medicine, Korea University, Seoul, Korea

T201

Analyzing the role of VE-cadherin tyrosine 658 for vascular permeability and leukocyte trans-migration in vivo

Astrid Fee Nottebaum1,FlorianWessel1, Takashi Sakurai1, Ute Ipe1,DietmarVestweber1

1Max-Planck-Institute For Molecular Biomedicine, Münster, Germany

• Mutation of VE-cadherin tyrosine 658 in vivodoesnotaffectpermeabilityinductioninaMilesAssay.

• Leukocytes extravasate normally into theinflamed cremaster of VE-cadherin-Y658F-KImice.

• Applicationof shear inducesphosphorylationofVE-cadherintyrosine658.

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T203

17β-Estradiol switches miRNA profile in human endothelial cells

Susana Novella1,DanielPerez-Cremades1, Xavier Vidal-Gomez1, Ana Mompeon1,AnaPaulaDantas2, Carlos Hermenegildo1

1University of Valencia and INCLIVA Biomedical Research Institute, Valencia, Spain, 2Institut Clinic Cardiovascular (ICCV) and Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain

• miRNAprofileinHUVECaremodifiedbyphysio-logicalconcentrationsof17β-estradiol.

• 17β-estradiol changes miRNA profile throughestrogen receptors.

• miRNA pathways linked to E2 provide newinsights by which estrogen can modulate theendothelialfunction.

T204

Noninvasive intravital 3D imaging of pancre-atic neuroendocrine tumor (PNET) growth and angiogenesis

Mirela Balan1,MartaAlabrudzinska1, Chenfei Ning1, Stefan Jacobs2, Daniel Nyqvist1

1Division of Vascular Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden, 2The Rolf Luft Research Center for Diabetes and Endocrinology, Karolinska Institutet, Stockholm, Sweden

• Newplatformfornoninvasiveintravital3Dimag-ing of pancreatic neuroendocrine tumor (PNET)biologyanddrugcandidateevaluation

• Rip1Tag2 (RT2) tumors implanted into the ante-rior chamber of the eye (AC) engraft and showcontinuoustumorgrowthandangiogenesis

• Intravital3Dimagingandquantificationoftumorgrowthandangiogenesis, intratumoral cell pop-ulations, drug efficacy and genetically modifiedgeneexpression

T205

ETV2-TET1/2 Complexes Induce Endothelial Cell-Specific Robo4 Expression via Promoter Demethylation

Toru Tanaka1,KoheiIzawa1,OsamuNakagawa2,WilliamAird3,HiroyukiMizuguchi1,KenjiKawabata4, Takefumi Doi1, Yoshiaki Okada1

1Osaka University, Suita, Japan, 2National Cerebral and Cardiovascular Center Research Institute, Suita, Japan, 3Beth Israel Deaconess Medical Center, Boston, USA, 4National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Japan

• Robo4promoterdemethylationandETV2expres-sionwereobservedduringendothelialcelldiffer-entiation.

• ETV2-TET1/TET2complexesdemethylatethepro-moterandinduceRobo4expression.

• 3.AnovelmechanismofEC-specificgeneexpres-sionviademethylationisproposed.

T206

SMAD4 prevents flow induced arterial-venous malformations by inhibiting Casein Kinase 2

Roxana Ola1, Anne Eichmann1

1Yale University, Cardiovascular Department, New Haven, USA

• Loss of Smad4 in endothelium results in AVM for-mationinhighflowregionssimilartoBMP9/10-Alk1deficiency.

• BMP9-ALK1 signaling antagonized flow-inducedAKTactivationinanALK1andSMAD4dependentmanner

• SMAD4isanessentialeffectorofBMP9-10/ALK1signaling thataffectsAVMpathogenesisvia reg-ulationofCK2expressionandPI3K/AKT1activa-tion.

T207

Propranolol Repurposing and High Through-put Screening for treatment of Cerebral Cav-ernous Malformation

Joppe Oldenburg1, Veronica Sundell1,CharlotteRorsman1, Johan Brännström1,PeetraMagnusson1,Prof.,ElisabettaDejana1

1Uppsala University, Uppsala, Sweden

• Cerebral Cavernous Malformation (CCM) treat-mentislimitedtosurgery,therapeuticdrugtreat-mentswouldbemorebeneficial

• PropranololcanreverseCCMEndothelialtoMes-enchymalTransition(EndMT)invitro,andreduceCCMlesionburdeninvivo

• High Throughput Screening, assay based onEndMTreversal,willrevealnovelsmallmoleculestobeusedforCCMtreatment

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T208

Expression of NOTCH3 and NOTCH target genes in CADASIL mutation carriers

Daniel V. Oliveira1, Sonja Bergmann1,MinhP.Vuong1, Raj N. Kalaria2, Kirsten G. Coupland1, Helena Karlström1

1Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden, 2Institute of Neuroscience, Campus for Ageing and Vitality, Newcastle University, Newcastle, United Kingdom

• Cerebral autosomal dominant arteriopathy withsubcortical infarcts and leukoencephalopathy(CADASIL) is themost common familial cerebralsmall vessel disease.

• NOTCH3,PDGFRβandHEYLexpressionwasele-vated inCADASIL compared tonormalbraintis-sue.HES1expressionwasreducedinCADASIL.

• WewillquantifybyWBNotch3andtargetgenesto determine whether altered gene expressioncorrelateswithproteininCADASILtissue.

T209

GATA4 and LMO3 balance angiocrine signal-ling and autocrine inflammatory activation by BMP2 in liver endothelium

Victor Olsavszky1,2,FriederikeUlbrich1,SandhyaSingh1,MiriamDiett1,CarstenSticht3,ChristianDavidSchmid1,2,JohannaZierow1,2,SebastianWohlfeil1,2, Kai Schledzewski1,2,StevenDooley4,HaristiGaitantzi4, Katja Breitkopf-Heinlein4,CyrillGéraud1,2, Sergij Goerdt1,2, Philipp-SebastianKoch1,2

1Department of Dermatology, Venereology and Allergy, University Medical Center and Medical Faculty Mannheim, University of Heidelberg, and Center of Excellence in Dermatology, Mannheim, Germany, 2European Center for Angioscience, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, 3Center for Medical Research, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, 4Department of Medicine II, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany

• GATA4 induces autocrine BMP2 signalling inendothelial cells

• GATA4-dependent BMP2 signalling leads toup-regulationofinterferon-associatedgenes

• GATA4-dependent, BMP2-mediated inflamma-tory endothelial activation is attenuated in liversinusoidalendotheliumbytranscriptionalregula-tor LMO3

T210

VEGFC Protects Against Glomerular Damage Caused By Diabetes And Endothelial Glycoc-alyx Loss

Karen Onions1, Nicola Buckner1, Siân Baker1, Monica Gamez1,KaiBetteridge1, Sara Desideri1, Raina Ramnath1, Chis Neal1,PeterMathieson1, Luigi Gnudi2, Kari Alitalo3, David Bates4,AndrewSalmon1,GavinWelsh1, Simon Satchell1,RebeccaFoster1

1Bristol Renal, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom, 2Cardiovascular Division, Faculty of Life Sciences & Medicine, Kings College London, London, United Kingdom, 3Molecular Cancer Biology Program, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland, 4Cancer Biology, Division of Cancer and Stem Cells, School of Medicine, University of Nottingham, Nottingham, United Kingdom

• VEGFC(exvivo)restoredalbuminpermeabilityin:VEGFAtreated(exvivo);anddiabeticglomeruli

• Overexpression of podocyte VEGFC in diabe-tes prevented albuminuria, kidney hypertrophy,GEnC fenestration loss and changes in VEGFreceptorexpression.

• VEGFCrestoredalbuminpermeabilityandmain-tainedtheeGLXinenzymaticallytreatedglomer-uli.

T211

Neutrophil extracellular traps (NETs) triggers atherosclerotic lesion development in high fat diet fed mice.

Mizuko Osaka1,MasayukiYoshida1

1Department of Life Sciences and Bioethics, Tokyo Medical And Dental University, Tokyo, Japan

• Activated neutrophil induce atheroscleroticlesion.

• Citrullinationof histoneH3 increased in aorta ofLDLR-/-micefedHFD.

• PlasmaofLDLR-/-micefedHFDinducedcitrulli-nationofneutrophils.

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T212

Mitochondrial inhibitory factor protein 1 antagonizes coupling factor 6-inducedδaging signal

Tomohiro Osanai1, Kasumi Mikami1, Maiko Kitajima1, ToshikoTomisawa1

1Department of Nursing Science, Hirosaki University Graduate School of Health Science, Hirosaki, Japan, ,

• We tested the hypothesis that mitochondrialinhibitory factor protein 1 (IF1) may attenuateCF6-induced aging signaling

• IF1inductionsuppressedCF6-inducedexpressionofaginghallmarkssuchastelomereattrition,epi-genetic alterations, defective proteostasis, andgenomicinstability.

• This provides understanding of the aging mecha-nism,andanoveltherapeutictargetforanti-ag-ingaswellasvascularmedicine.

T213

Piezo1 Cation Channels Mediate Uterine Artery Endothelial Shear Stress Mechano-transduction and Vasodilation During Preg-nancy

George Osol1, Liam John1, Natalia Gokina1, Nga Ling Ko1

1Univ Vt Coll Med, Burlington, United States

• Increased uteroplacental blood flow is essentialfornormalpregnancyoutcome,andismediatedby increased shear stress and endothelial nitricoxideproduction.

• The molecular mechanosensor(s) that links these processesisnotknown.

• WepresentthefirstevidencethatindicatesthatPiezo1, a novel cation channel, plays a primaryphysiologicalroleinthisvasodilatoryprocess.

T214

The particular glycomes of lymph node lym-phatic endothelia may determine the localiza-tion of siglec-1+ macrophages

Marco D’Addio1, Catharina Commerford1,JasminFrey1, Richard D. Cummings2, Michael Detmar1, Vivianne I. Otto1

1ETH Zurich, Zurich, Switzerland, 2Harvard Medical School, Boston, USA

• There are clear differences between the gly-comes of human lymphatic and blood vascularendothelial cells.

• Withinmouselymphnodes, lymphaticendothe-lial cellsof thesubcapsularsinus (SCS)displayadistinctiveglycosylationpattern.

• TheglycanspresentonSCSfloorlymphaticendo-thelialcellsmaybeofimportanceforthelocaliza-tionofsiglec-1+macrophages.

T215

Notch1 signaling induces pathological vascu-lar permeability in diabetic retinopathy

Malika Oubaha1, Khalil Miloudi2, Catherine Ménard3, Agnieszka Dejda3,VeraGuber3, Gael Cagnone5, Ariel Wilson1,GaelleMawambo1,RonyChidiac5, Chantal Delisle5,KatieBentley,Jean-SebastienJoyal5, Flavio Rezende Rezende3,FréderickAntoineMalette1,4, Jean-PhilippeGratton5, Bruno Larivée3,PrzemsyslawSapieha1,2,3

1Department of Biochemistry, Maisonneuve-Rosemont Hospital Research Centre, University of Montreal, Montreal, Canada, 2Department of Neurology-Neurosurgery McGill University, Montreal , Canada., 3Department of Ophthalmology, Maisonneuve-Rosemont Hospital Research Centre, University of Montreal , Montreal, Canada, 4Department of Medicine, Maisonneuve- Rosemont Hospital Research Centre, University of Montreal, Montreal, Canada, 5Department of Pharmacology and Physiology, University of Montreal, Montreal, Canada

• Notch1signaling inmaturediabeticretinascon-tributestoincreasedvascularpermeability.

• Jagged1 and Delta Like-4 are upregulated in hyperglycemia and activate a non-canonicalNotch1 leading to endothelial adherens junc-tionsdisruptionbydissociatingVE-cadherinfromb-catenin.

• NeutralizationofNotch1ligandspreventsdiabe-tes-inducedretinaledemaasdoestargetedcon-ditional knockdown of Notch1 and could be aninterestingtherapeuticavenue.

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T216

High-resolution intravital imaging of tumour cell extravasation

Ilkka Paatero1,GuillaumeJacquemet1, Johanna Ivaska1

1Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland

• Mammalian cancer cells can be xenografted tozebrafishembryos

• Zebrafishembryosareagoodmodelforhigh-res-olutionintravitalimagingofvasculature.

• Extravasationcanbestudiedindetailusingintra-vitalimagingofxenograftedzebrafishembryos.

T217

One year experience of new histopathologic consensus grading system in surgical aortic specimens

Timo Paavonen1,2,SakuPelttari1,2, Ari Mennander3, Ivana Kholová1,2

1University of Tampere, Tampere, Finland, 2Department of Pathology, Fimlab Laboratories, Tampere, Finland, 3Heart Center, Tampere University Hospital, Tampere, Finland

• A new consensus statement was designed byHalushkaetal tounifythenomenclatureofhis-topathological changes in the noninflammatorydegenerativeaorta.

• Weanalyzed andgradedall aortic samplespro-cessed during 2016 at our Department.

• Thegradingsystemwaswellreceivedbypathol-ogistsandeasilyadopted,andithelpedcommu-nication between clinical and pathology depart-ments.

T218

Triptolide dual targeting YAP signaling and b-FGF-dependent vascular niche reduces hepatic metastasis in uveal melanoma

Jingxuan Pan,Mr.FuxingTan1Sun Yat-sen University Zhongshan Ophthalmic Center, Guangzhou, China

• Triptolide effectively inhibited malignancy ofuvealmelanoma cells through blocking YAP sig-naling.

• Triptolideprofoundlyabolishedhepaticmetasta-sis in uveal melanoma.

• Triptolide treatmentdisturbedongiocrine secre-tionofb-FGFand itsdependentangiogenesis inuveal melanoma.

T219

IL-6 trans-signaling in vascular endothelial cells regulates proteins involved in inflamma-tion, fibrinolysis and vascular calcification

Mulugeta Zegeye1,AshokKumawat1, Allan Sirsjö1, Liza Ljungberg1

1Örebro University, Örebro, Sweden

• IL-6 trans-signaling in human vascular endothelial cells causes release of chemoattractants CCL2,CXCL16, CCL15 and IL-1RT1.

• It also leads to release of proteins including TR-AP,IL-18BP,andOPGthatareassociatedwithpromotionofvascularcalcification.

• Moreover, it downregulates the production ofuPAandtPAwhichareproteinsinvolvedinfibri-nolysis.

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IVBM2018

W001

Marathon improved central blood pressure, augmentation index, and endothelial progeni-tor cells

Jae Hyoung Park1

1Korea University, , South Korea

• Marathon• Centralbloodpressure• Endothelial progenitor cells

W002

Exercise improved flow mediated dilation after Big Mac diet compared with Korean food.

Jae Hyoung Park1,Hyo-JungNam2

1Korea University, , South Korea, 2Asan Medical Center, , South Korea

• Exercise• Flowmediateddilation• Vascular aging

W003

Hecw2 controls YAP/TAZ activities by stabiliz-ing AMOTL1

Jeong Ae Park,Kyu-SungChoi,Young-GuenKwon1Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, Seoul, South Korea

• Hecw2 enhances endothelial cell-to-cell junc-tions through the regulation of AmotL1 proteinstabilityviaK63-linkedubiquitination.

• Disruption of Hecw2-mediated AmotL1 stabilityincreasesYAP’snuclearactivity,therebypromot-ingECsproutingviaangiopoietin-2expression.

• Hecw2 plays a significant role in lung develop-ment.

W004

Endothelial protein tyrosine phosphatase improves vascular inflammation through the A20-mediated NF-κB inactivation

ByungtaeHwang1, Jong-gil Park1, Jeong-ki Min1,2

1Korea Research Institute Of Bioscience & Biotechnology, Daejeon, South Korea, 2University of Science & Technology, Daejeon, South Korea

• ePTP on endothelial cells regulated the expres-sion of cytokines-mediated cell adhesion mole-cules including ICAM-1 and VCAM-1.

• A20-mediatedinactivationofNF-kBsignalingwasresponsibleforanti-inflammatoryeffectsofePTPon endothelial cells.

• ePTPoverexpressioninendotheliumamelioratedthe development of atherosclerosis in ApoE KO mice fed HFHC.

W005

Contributing factors for the short-term pro-gression of carotid plaque and its correlation with clinical outcomes

Kyu-hwan Park1,Sang-WookKang1,Jeong-HwanCho1

1Daegu Veterans Hospital, Daegu, South Korea

• Cardiovascular events were relatedwith plaqueprogressionevenin1-yearfollow-upperiod

• Risk factors for cardiovascular events: Plaqueprogression,BMI<23kg/m2,underlyingcoronaryarterydisease

• Risk factors for carotid plaque progression: Thepresenceofcarotidplaqueattheindexexamina-tionandahistoryofcoronaryarterydisease


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W006

Angiopoietin-2 unfavorably modifies cardiac vessels and macrophages after myocardial infarction

Intae Park1,2, Seung-Jun Lee2, Choong-Kun Lee1,2, Seok Kang1,SeonPyoHong2, Hosung Bae1,2,YulongHe3,YoshiakiKubota4,GouYoungKoh1,2

1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea, 2Center for Vascular Research, Institute for Basic Science, Daejeon, South Korea, 3Cyrus Tang Hematology Center, Soochow University, Suzhou , China, 4The Laboratory of Vascular Biology, School of Medicine, Keio University, Tokyo , Japan

• During acute myocardial infarction, Angpt2antagonizes Angpt1-Tie2 signaling to induce det-rimentalchangesincardiacvesselsininfarctbor-der area.,

• Duringchronicmyocardialinfarction,Angpt2pro-motesabnormalvascularremodelingandproin-flammatory macrophage polarization to worsencardiachypoxiaandinflammation.,

• Genetic or therapeutic anti-Angpt2 alleviatessuchadverseeventsandoffersbeneficialconse-quences in post-ischemic cardiovascular remod-eling.

W007

TrxR1 expression is increased by Korean Red Ginseng in human endothelial cells

Hye Rim Park1,SeungEunLee1,HyemiKim1, Seeun Jeon1, DongkyoHan1,YongSeekPark1

1Kyung Hee University, Dongdaemun-gu,, South Korea

• Endothelial cells• Thioredoxinreductase1• Korean Red Ginseng

W008

Right ventricular analysis using real time three-dimensional echocardiography for the dependency of preload changes

Chan Seok Park1

1Catholic University of Korea, Seoul, South Korea

• Preload• Right ventricle• Strain

W009

Vascular Stiffness Measured by Circumferen-tial Strain of Carotid Artery is Deteriorated in Naive Non-dippers.

Chan Seok Park1

1Catholic University Of Korea, Seoul, South Korea

• Vascularstiffness• Strain• Hypertension

W010

Relationship between dyslipidemia and short stature in adolesents and adults; from the Korean NHANES survey

Mi-Jung Park1,Shin-HyeKim1

1Inje University, Paik Hospital , Seoul, South Korea

• Weanalyzed37,889KoreandatafromKNHANES.• Total cholesterol, triglycerides and LDL-choles-

terol concentrations were inversely associatedwithheight.Theoddsratiosforhypercholesterol-emia,hypo-HDL-cholesterolemia,hypertriglyceri-demia, andhyper-LDL-cholesterolemiawere sig-nificantlyincreasedinshortstature.

• Theriskofdyslipidemiaissignificantly increasedin individuals with short stature. These resultsimplicate the mechanism of increased cardiovas-cular risk in short stature.

W011

Bioactive sphingolipid ceramide-1-phosphate (C1P) prevents ovarian aging by improving microvasculature

LeopoldinaScotti1, Natalia Pascuali1,GonzaloOubiña1, AgustinaMena2,DalhiaAbramovich1,SoledadNegrotto2, FernandaParborell1

1Institute of Biology and Experimental Medicine (IByME - CONICET), Buenos Aires, Argentina, 2Institute of Experimental Medicine - National Academy of Medicine, Buenos Aires, Argentina

• Endothelialprogenitorcells(EPCs)weredetectedinperipheral blood7dayspostC1Padministra-tioninagedmiceovaries.

• C1PincreasedtheperiendothelialcellsareaandVEGF-A levels in ovaries from aged mice.

• C1P in FF from aged patients increased theendothelial cellsmigrationbuthadnoeffectonVEGF-A levels.


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IVBM2018

W012

Characterization of novel angiogenic factors implicated in ovarian hyperstimulation syn-drome (OHSS): potential vascular hyperper-meability treatment?

Natalia Pascuali1,LeopoldinaScotti1,GonzaloOubiña1, IgnaciodeZúñiga2, Marta Tesone1, Dolores Busso3, Dalhia Abramovich1,FernandaParborell1

1Institute of Biology and Experimental Medicine (IByME-CONICET), Buenos Aires, Argentina, 2PREGNA Medical Centre, Buenos Aires, Argentina, 3Department of Nutrition, Diabetes and Metabolism, Faculty of Medicine, Pontifical Catholic University of Chile, Santiago, Chile

• Disrupted balance between ovarian pro- andanti-angiogenicfactors,withconsequentvascularleakage, lead toOHSS onset in hormone-stimu-latedwomen.

• Follicular fluids from OHSS patients havedecreased PDGF-B, PDGF-D, PDGFRβ, S1P andaltered HDL composition compared to controlpatients.

• PDGF-B administration increases perivascularcoverage, claudin-5 and N-cadherin expressionanddecreasesvascularhyperpermeabilityinova-ries from OHSS rat model.

W013

Immunosuppression agent cyclosporine reduces in vivo progenitor and functional capacity of endothelial colony forming cells

Jatin Patel1,2, Seen-Ling Sim1,2,JosueAlexis2,AbbasShafiee1,HoYiWong1,2, Kiarash Khosrotehrani1,2

1The University Of Queensland Diamantina Institute, Brisbane, Australia, 2The University of Queensland Centre for Clinical Research, Brisbane, Australia

• CyclosporinereducedtheinvivofunctionofECFCby inhibiting de novo vessel formation wheninjected into the host

• Cyclosporinereducedinvitroprogenitorcapacityof ECFCbypreventingclonality and slowing cellgrowth

• Immunosuppression could adversely be impact-ing allogeneic stem cells being used in treatingischemic disease

W014

Endovascular progenitors initiate and drive de novo vascularisation in melanoma

Jatin Patel1, James Dight1,PrudenceDonovan1,HoYiWong1, Seen-Ling Sim1, Kiarash Khosrotehrani1

1The University Of Queensland Diamantina Institute, Brisbane, Australia

• Identified a novel vascular resident progenitorpopulation (EVP) that migrate into tumors anddrivesdenovovesselformation

• RNA-seqdemonstrated JAK/STAT andNotch sig-nallingtobekeyregulatorsofEVPfunctioninthetumor environment

• Blocking JAK/STAT or Notch signalling reducedEVP penetrance into the tumor, resulting in areducedvesselnetwork

W015

Endothelial cells negatively modulate cell proliferation and ROS in smooth muscle cells from hypertensive rat

Michele Paulo1, Marcella Daruge Grando1, Juliana Aparecida Vercesi1, Lusiane Maria Bendhack1

1Faculty Of Pharmaceutical Sciences Of Ribeirão Preto-usp, Ribeirao Preto, Brasil

• Co-culture of EC-VSMCs increases NO in VSMC from 2K-1C rat aortas

• ECsdecreaseROSproductioninVSMCs• ECs decrease proliferating cell nuclear antigen

(PCNA)expressionandVSMCsproliferation

W016

Loss of the transcription factor ERG leads to impairment of Thrombomodulin-Protein C system and thrombosis

Claire Peghaire1,NeilDufton1, Miss Marie Lang1,IsabelleSalles-Crawley2,JosefinAhnströem2, Miss Viktoria Kalna1, CharisPericleous1, Claudio Raimondi1,GraemeBirdsey1, JustinMasson1, Anna Randi1

1Imperial College London, National Heart & Lung Institute, Vascular Science, , United Kingdom, 2Imperial College London, Center for Hematology , London, United Kingdom

• The endothelial transcription factor ERG regu-latesThrombomodulinlevelsandactivityinvitroand in vivo

• LossofERGinadultmiceisassociatedwithspon-taneousthrombusformationinliverandhaemor-rhagesinliverand/orlung

• 50% of ErgiEC-KO mice show reduced plateletscountandincreasedD-dimerplasmalevelshow-ingthatlossofERGleadstocoagulopathy


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IVBM2018

W018

A role for endothelial Pentraxin 3 in the patho-genesis of diabetic retinopathy

Elisa Peixoto1,Lynsey-DawnAllen1,VarunPathak1,PietroMaria Bertelli1,ChristinaO`Neill1, Kiran McLoughlin1, Allan Stitt1, Reinhold Medina1

1Centre for Experimental Medicine, School of Medicine, Dentistry, and Biomedical Science, Queen’s University Belfast, Belfast, United Kingdom

• Pentraxin3protein levels inplasmasignificantlyincreaseindiabeticmice.

• Pentraxin 3 mRNA expression is significantlyupregulated inendothelialcellsexposedtohighglucosefor7days.

• Pentraxin3inhibitsFGF-inducedendothelialtubeformationinvitro.

W019

Targeting VEGFR2’s interaction with the adap-tor molecule TSAd to suppress vascular per-meability

Tor Persson Skare1,FrancisPeterRoche1, Daisuke Fukuhara1,ElisabetOhlinSjöström1,ElinSjöbergHägerstrand1,LenaClaesson-Welsh1

1IGP, Uppsala University, Uppsala, Sweden

• Excess vascular permeability is an importantpathologicalfeatureinmanydiseases

• Phosphorylated Y949 in VEGFR2 binds TSAdwhichviac-Srccauses internalizationofVE-Cad-herinandconsequentvascularpermeability

• Usingacombinationofinvitroandinvivometh-odswe aim to target the VEGFR2-TSAd interac-tionforfuturetherapeuticpurposes

W020

Endothelial cell function is controlled by the age and shear stress regulated lncRNA Aerrie

Phat Pham1,DiewertjeBink1,PatrickHofmann2, Laura Stanicek1,2,LjubicaPerisic3, Ulf Hedin3, Stefanie Dimmeler2, Reinier Boon1,2

1Department of Physiology, Amsterdam Cardiovascular Sciences, VU University Medical Center, Amsterdam, Netherlands, 2Institute of Cardiovascular Regeneration, Goethe University, Frankfurt am Main, Germany, 3Vascular Surgery Division, Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden

• Lowshearstressandageingaffectcardiovascularfunctionandincreasesendothelialdysfunction

• Ageing and shear stress regulate lncRNA Aerrie• LncRNAAerriecontrolssprouting,migration,and

barrierfunctioninendothelialcells

W021

T-cadherin in pericyte function: a novel molec-ular mechanism regulating endothelial-peri-cyte interactions.

Mr. Boris Dasen1, Therese J. Resink2,PaulErne2, Olga RiveroMartín3,Klaus-PeterLesch3,IvanMartin1, Maria Philippova1

1Tissue Engineering Lab, Departments of Biomedicine and Surgery, Basel University Hospital, Basel, Switzerland, 2Signaling Lab, Department of Biomedicine, Basel University Hospital, Basel, Switzerland, 3Division of Molecular Psychiatry, University of Würzburg, Würzburg, Germany

• Atypical adhesion molecule T-cadherin isexpressedinmicrovascularpericytesfromdiffer-enttissues.

• T-cadherinregulatespericyteproliferation,migra-tion, invasion and interactions with endothelialcells during angiogenesis.

• T-cadherin modulates expression of pericytegenes relevant for angiogenesis, inflammationanddifferentiation.

W022

Perivascular macrophages regulate blood flow following tissue damage

Evelina Vågesjö1, Cedric Seignez1,GustafChrsitoffersson1, Carmen Herrera Hidalgo1, Antoine Giraud1, Olle Korsgren1, HeleneRundqvist2, Magnus Essand1, Lena Holm1, Randall Johnson2, Mia Phillipson1

1Uppsala University, Uppsala, Sweden, 2Karolinska Institute, Stockholm, Sweden

• Macrophages accumulate perivascularly in isch-emictissues

• Perivascularmacrophagesregulatebloodflowinischemictissuesbyproducingnitricoxide

• CXCL12 overexpression in ischemic tissuesincreased the number of perivascular macro-phages,resultinginimprovedbloodflowregula-tionandlimbfunction


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IVBM2018

W023

Substance P ameliorates tumor necrosis fac-tor-alpha-induced endothelial cell dysfunction by regulating eNOS expression

Jiyuan Piao1,HyunSookHong2,YoungsookSon1

1Graduate School of Biotechnology, Kyung Hee University, Yong In, Republic of Korea, 2Department of Biomedical Science and Technology, Graduate School / East-West Medical Research Institute, Kyung Hee University, Seoul, Republic of Korea

• TNF- α-induced cell death is occurred due to NO deficiency

• SPcanenhanceeNOSexpressionandNOsecre-tioninHUVEC

• SP-mediatedAkt/eNOS/NO signaling contributestocellularprotectionagainstTNF-α

W024

Endothelial cell-derived Shb as a mediator of VEGFR2- and FAK- signaling.

Ilkka Pietilä1,MichaelWelsh1

1University Of Uppsala, Uppsala, Sweden

• Shb is an adapter protein that conveys signalsdownstreamofseveraltyrosinekinasereceptors.

• AfterVEGFstimulationVEGFR2/FAKandShb/FAKassociatenear thebasalplasmamembraneandplasmamembranejuxtaposedVEGFR2/Shbcom-plexdissociates.

• The data suggest that we can target signalingcascades operating at specific intracellular sitesby finding chemical inhibitors that inhibit Shb/VEGFR2orShb/FAKassociation.

W025

Paladin (Pald1) is a phosphatidylinositol phos-phatase regulating VEGFR2 trafficking and signaling

Anja Nitzsche1,6,ChiaraTestini1, Riikka Pietilä1,ElisabethEkvärm1,JimmyLarsson1,KatieBentley1,2,AndrewPhilippides1,3,FrancisP.Roche1,IsabelEgaña1, Ross Smith1, CarinaHellberg4, Kurt Ballmer-Hofer5,PhilippBerger5, Mats Hellström1

1Department of Immunology, Genetics and Pathology, The Rudbeck laboratory, Uppsala University, Uppsala, Sweden, 2Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harward Medical School, Boston, USA, 3Centre for Computational Neuroscience and Robotics, Department of Informatics, University of Sussex, Brighton, UK, 4Ludwig Institute for Cancer Research, Uppsala University, Uppsala, Sweden, 5Paul-Scherrer Institute, Biomolecular Research Molecular Cell Biology, Villingen-PSI, Switzerland, 6INSERM U970, 56 rue Leblanc, F-75015, Paris, France

• to study mechanistically the role of Paladin(Pald1) inVEGFR2signallingandendothelialcellbiology

• Paladin regulates VEGFR2 signalling via recep-tor trafficking and in vivo lossof paladin affectsendothelialsproutingandpermeability

• PaladinisanovelregulatorofVEGFR2signalling

W026

Kindlin-2 as a regulator of the vascular barrier function of endothelial cells.

Edward Plow1, Dorota Szpak1,ElzbietaPluskota2

1Cleveland Clinic, Cleveland, United States, 2Lerner Research Institute, Cleveland Clinic , Cleveland, United States

• Kindlin-2 is present in adherens junctions ofendothelial cells.

• Kindlin-2interactswithβ- and γ-cateninandactinwithinadherensjunctions

• Kindlin-2contributestovascularbarrierfunctionof endothelial cells.


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IVBM2018

W027

Lack of miR-378 attenuates dystrophic phe-notype in mdx mice

Paulina Podkalicka1, Olga Mucha1, Magdalena Kozakowska1,KatarzynaPietraszek-Gremplewicz1,IwonaBronisz-Budzynska1,JerzyOstrowski2,3, Michal Mikula3, AlicjaJozkowicz1,AgnieszkaLoboda1, Jozef Dulak1

1Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland, 2Department of Genetics, Maria Sklodowska-Curie Memorial Cancer Center and Institute of Oncology, Warsaw, Poland, 3Department of Gastroenterology, Hepatology and Clinical Oncology, Centre of Postgraduate Medical Education, Warsaw, Poland

• SeverityofDuchennemusculardystrophy,adis-ordercausedbythelackofdystrophin,isaffectedbymicroRNAs,includingmiR-378.

• Lack of miR-378 in dystrophic mice leads toimproved running capacity followed by, amongothers,decreasedinflammationandfibrosis.

• Transcriptome-based analysis revealed FGF1 asoneofthemostdownregulatedgenesindystro-phic mice lacking miR-378.

W028

Dual anti-platelet effect in the ADP-induced model of non-lethal pulmonary thromboembo-lism in mice

Dawid Polak1, Marcin Talar1,TomaszPrzygodzki1,CezaryWatala1

1Department of Haemostatic Disorders, Chair of Biomedical Sciences, Faculty of Health Sciences, Medical University of Lodz, Lodz, Poland

• Dualanti-plateleteffectofA2AreceptoragonistandP2Y12receptorinhibitorintheADP-inducedmurinemodelofnon-lethalpulmonarythrombo-embolism

• InhibitorofP2Y12receptoralleviatedadecreasedbloodflowrate.AdministrationoftheagonistofA2Areceptordeepenedthiseffect.

• CombinationofA2AreceptoragonistandP2Y12receptor inhibitor seems promising potentialstrategyfornovelanti-plateletagents

W029

Sphingosine-1-phosphate (S1P) signaling regulates reverse transendothelial migration (RTM) of aortic intimal dendritic cells (DCs)

Chanele Polenz1,2,MyronCybulsky1,2

1Department of Laboratory Medicine & Pathobiology, University of Toronto, Toronto, Canada, 2Toronto General Research Institute, University Health Network, Toronto, Canada

• RTMof intimalDCs into thecirculation isapro-tective immune response, triggeredby systemicadministrationoflipopolysaccharide(LPS).

• LPS upregulates S1P receptor expression andpharmacological inhibition of S1PR1 and S1PR3blocksLPS-inducedRTMofintimalDCs.

• LPS-induced RTM does not occur in mice defi-cientinSPHK1,anS1P-producingenzyme.

W030

Study of the crosstalk between VEGF and BMP9 pathways: implications in Hereditary Hemorrhagic Telangiectasia

Thomas Pollenus1, Ingrid Struman1

1Uliège - Giga Research, Liège, Belgium

• Angiogenesis• SignallingandTrafficking• HereditaryHemorrhagicTelangiectasia

W031

HÉMO-IONIC®, a new hemostatic, shows vascular regeneration properties by activating endothelial cells

Anne-Charlotte Ponsen1,2,RichardProust1,LaetitiaBoutin4, Oriane Guillevic3, Florence Armstrong3, Georges Uzan1,JeanJacquesLataillade1,4

1INSERM UMR 1197, Villejuif, France, 2Université Paris Sud - Paris Saclay - Faculté de pharmacie, Chatenay-Malabry, France, 3Les Laboratoires BROTHIER, Nanterre, France, 4Centre de Transfusion Sanguine des Armées, Clamart, France

• HÉMO-IONIC®,anewhemostatic,actspositivelyon platelets favoring a better hemostasis com-paretohemostaticscurrentlyuseinsurgery

• Only HÉMO-IONIC® preserves endothelial cellintegrityandincreasestheirmigratoryability

• HÉMO-IONIC® is the only agent tested showingangiogenicproperties


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IVBM2018

W032

Role of mesenchymal stem cells in the devel-oping tissue engineered vascular graft on poly(L-lactide) scaffold

Gury Popov1,2,PavelPopryadukhin2,3,GalinaYukina1,2, Irina Dobrovolskaya2,3,ValeriyVavilov1,VladimirYudin1,2

1First Pavlov State Medical University, Saint-Petersburg , Russian Federation, 2Peter the Great Saint-Petersburg State Polytechnical University, Saint-Petersburg , Russian Federation, 3Institute of Macromolecular Compounds, Russian Academy of Sciences, Saint-Petersburg , Russian Federation

W033

Caveolae number is reduced in mesenteric arteries of spontaneously hypertensive rats

Simone Regina Potje1, Marcella D Grando1, Juliana A Vercesi1, Andreia Z Chignalia2,CristinaAntoniali3, Lusiane M Bendhack1

1Faculty of Pharmaceutical Sciences of Ribeirão Preto - USP, Ribeirão Preto, Brazil, 2College of Medicine - UIC, Chicago, United States, 3School of Dentistry - UNESP, Araçatuba, Brazil

• Caveolaenumber is lower inSHRthan inWistarrat mesenteric arteries

• Caveolae structure contributes to endotheli-um-dependent relaxation in normotensive andhypertensiverats

• Caveolae disassembled is associated withincreasedperoxynitriteproduction

W034

Plasminogen Activator Inhibitor-1 Promotes Neutrophil Infiltration and Tissue Injury on Ischemia-Reperfusion.

Marc Praetner1,2,GabrieleZuchtriegel1,MartinHolzer1,3, Bernd Uhl1,3,JohannaSchaubächer1,LauraMittmann1, MatthiasFabritius1, Stefan Zahler4, Stefan Zahler5, Dominik Funken1,6,MaximilianLerchenberger1,6, Andrej Khandoga1,6, Sandip Kanse7,KirstenLauber8, Fritz Krombach1, Christoph A. Reichel1,3

1Walter Brendel Center For Experimental Medicine, Munich, Germany, 2Department of Psychiatry and Psychotherapy, University Clinic, Friedrich-Alexander-University of Erlangen-Nuremberg, Germany , Erlangen, Germany, 3Department of Otorhinolaryngology Head and Neck Surgery , Munich, Germany, 4Institute of Pharmaceutical Biology, Goethe University Frankfurt, Germany , Frankfurt, Germany, 5Pharmaceutical Biology, Department of Pharmacy, Center for Drug Research, Munich, Germany, 6Department of Surgery LMU, Munich, Germany, 7 Institute of Basic Medical Sciences, University of Oslo, Norway , Osla, Norway, 8Department of Radiation Oncology Ludwig-Maximilians-Universität München, Munich, Munich, Germany

• Plasminogen activator inhibitor-1 (PAI-1) rapidlyaccumulatesontheendotheliumofthepostisch-emic microvasculature.

• Deposited PAI-1 subsequently directs neutro-phils to postischemic tissue by inducing affinitychanges in integrins of these immune cells via interaction with low-density lipoprotein recep-tor–relatedprotein-1andmitogenactivated

• Proteinkinases–dependentsignalingpathways.• DeficiencyofPAI-1effectivelyreversesischemia–

reperfusioninjurywithoutexhibitingsideeffectson microvascular hemostasis.

W035

Oxidative modifications in coronary circulation of Tgαq*44 mice during heart failure progres-sion assessed using IST

Bartosz Proniewski1,JoannaCzarny1, Tamara Khomich2, AgnieszkaZakrzewska1, Stefan Chlopicki1,3

1Jagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland, 2Institute of Pharmacology and Biochemistry, NAS of Belarus, Grodno, Belarus, 3Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland

• Oxidativemodificationsoccurlaterthansuperox-ideis increased,andbettercorrespondwiththefirstsymptomsofheartfailure

• Coronary circulation and cardiomyocytes areconcurrentlyaffectedbyoxidativemodifications,despite cardiomyocyte-specific origin of heartfailure in Tgαq*44mice

• Cardiomyocyte-derived mechanism responsiblefor coronary capillaries damagemay contributeto the progression of heart failure in this model


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IVBM2018

W038

Dach1 regulates arterial specification and col-lateral artery formation

Brian Raftrey1

1Stanford University, Stanford, United States

• Endothelial over expression of Dach1 increasedarterialcoverageanddensityofthecoronaryvas-culature

• Dach1 increased expression of arterial markersanddecreasedexpressionofvenousmerkers

• Over expression of Dach1 during developmentcausedcoronarycollateralarteryformation

W039

High-Throughput permeability assay on per-fused 3D microvessels in vitro

V. van Duinen2, C. Ramakers1, S.J. Trietsch1, A.J. van Zonneveld3, T. Hankemeier2,P.Vulto1

1Mimetas, Leiden, Netherlands, 2Division of Analytical Biosciences LACDR, Leiden University, , Netherlands, 3Department of Nephrology, Leiden University Medical Center, Leiden, Netherlands

• 96perfusedbloodvesselsonaplate• Long-termcultureviability(60days)• Invivo-likebarrierfunction

W040

Perfusable 3D angiogenesis in high through-put microfluidic culture platform

V. van Duinen2, C. Ramakers1, S.J. Trietsch1, A.J. van Zonneveld3, T. Hankemeier2,P.Vulto1

1Mimetas, Leiden, the Netherlands, 2Division of Analytical Biosciences LACDR, Leiden University, Leiden, the Netherlands, 3Department of Nephrology, Leiden University Medical Center, Leiden, the Netherlands

• Tip cells induction andmigration and stalk cellsformation

• Long term stable gradient in organ-on-a-chipplatform

• PerfusablecapillarynetworkthroughECM

W041

BBB on-a-chip: a 3D in vitro model of the human blood brain barrier (BBB)

N.R.Wevers1, X. Spijkers1, C. Ramakers1,K.J.Wilschut1, R. van Vught1, S.J. Trietsch1,P.Vulto1, J. Joore1

1Mimetas, Leiden, Netherlands

• HumanBBBmodelinOrgan-on-a-Chipplatform• 40 perfusedminiaturized BBB tissues with con-

firmedbarrierfunction• FunctionalityoftwomajorBBBtransporters,Pgp

and GLUT1

W042

Non-catalytic function of PI3Kg on smooth muscle cells proliferation during arterial remodeling through cAMP modulation.

Damien Ramel1, Adrien Lupieri1, Alessandra Ghigo2, Regis Blaise3, Natalia Smirnova1, Nicole Malet1,IsabelleLimon3, PierreVincent3,StéphanieGayral1, Emilio Hirsch2, Muriel Laffargue1

1Department of vascular biology of I2MC, INSERM UMR 1048, Toulouse, France, 2Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of torino, Torino, Italy, 3Sorbonne Universités, UPMC CNRS UMR 8256, Paris, France

• Non-catalytic functionof PI3Kg controls smoothmusclecellsproliferation

• PI3KgcontrolsPDEactivity• 3.BlockingPI3Kgdockingfunctionisanovelther-

apeutictargettopreventarterialremodeling

W043

Hypermuscularization of precapillary arteri-oles plays a critical role in spontaneous deep intracerebral hemorrhage

Julien Ratelade1, Valérie Domenga1, Anne Joutel1

1Inserm U1161-Université Paris Diderot, Paris, France

• Evidence for smooth muscle cell degenerationinarteriesandhypermuscularizationofprecapil-laryarteriolesinageneticmodelofintracerebralhemorrhage

• Genetic correction of hypermuscularization ofprecapillaryarterioles,withoutaffecting smoothmuscle cell loss in arteries, protects against intra-cerebralhemorrhage

• Micewithmuralcelllossinbotharteriesandpre-capillaryarteriolesareprotectedagainstintrace-rebralhemorrhage


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IVBM2018

W044

Novel activating proteases uncover new roles for VEGF-C

Khushbu Rauniyar1,SawanJha1,EwaChronowska4, Hannu Koistinen5, Ulf-Håkan Stenman5, Kari Alitalo1,2,3, Michael Jeltsch1,2

1Translational Cancer Biology Research Program, University Of Helsinki, Helsinki, Finland, 2Wihuri Research Institute, Helsinki, Finland, 3Helsinki University Central Hospital, Helsinki, Finland, 4Jagiellonian University Medical College , Cracow, Poland, 5Department of Clinical Chemistry, University of Helsinki, Helsinki, Finland

• Pro-VEGF-C becomes activated during the pro-teolyticcascadeofsemenliquefactionandactiveVEGF-Cincreasesspermmotility.

• KLK3activationofVEGF-Csynchronizesthejump-startofspermmotilitywithsemenliquefaction.

• The CCBE1 protein, which is necessary for effi-cientcleavageofVEGF-CbyADAMTS3,alsoaccel-erates KLK3-mediated cleavage of VEGF-C.

W045

Broad-spectrum chemokine inhibition blocks inflammation-induced pathological angiogen-esis but preserves hypoxia-driven physiologi-cal angiogenesis

Dhanya Ravindran1,2, Sian Cartland1,2, Joanne Tan3, ChristinaBursill3,MaryKavurma1,2

1Heart Research Institute, Sydney, Australia, 2University of Sydney, Sydney, Australia, 3South Australian Health and Medical Research Institute, Adelaide, Australia

• Broad-spectrum chemokine inhibition by ‘M3’proteinpreservedphysiologicalangiogenesisfol-lowingischaemicinjury

• M3inhibitedpathologicalangiogenesisfollowinginflammation-inducedinjury

• M3 reduced inflammation-inducedproliferation,migrationandtubuleformationinvitro,buthadnoeffectunderhypoxicconditions

W046

Encyclopedia of the molecular mechanisms involved in the arterial healing.

Anton Razuvaev1,LjubicaMaticPerisic1, Urszula Rykaczewska1, Bianca Suur1, Till Seime1, Samuel Röhl1, Maria Gonzalez Diez1, Anders Hamsten1,PerEriksson1, Ulf Hedin1

1Karolinska Institutet, , Sweden

• We created a biobankwith genome-wide longi-tudinalanalysisofthemolecularmechanismsofthevascularhealingreaction.

• Transcriptomic analysis with morphological vali-dationwasperformedontheinjuredratarteriesatvarioustimepoints(minutestoweeks).

• The data is being prepared for public releaseallowing the research community to use thisuniquebiobankinfuturestudies.

W047

Endoglin as a putative cellular receptor to mediate anti-angiogenic effects of SPARCL1

Daniela Regensburger1, Victoria Langer1, Clara Tenkerian1, HeinrichSticht2, Andreas Ramming3,ThomasWohlfahrt3, Benjamin Schmid4, Valérie Méniel5,RobertGrützmann6, Michael Stürzl1,ElisabethNaschberger1

1Division Of Molecular And Experimental Surgery, Translational Research Center, Department of Surgery, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany, 2Insitute of Bioinformatics, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany, 3Department of Rheumatology and Immunology, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany, 4Optical Imaging Center Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany, 5European Cancer Stem Cell Research Institute, Cardiff University, CF24 4HQ Cardiff, United Kingdom, 6Department of Surgery, University Medical Center Erlangen, Friedrich-Alexander-University Erlangen-Nuremberg, 91054 Erlangen, Germany

• SPARCL1 paracrinely inhibits sprouting of wild-typemetatarsalsexvivo.

• SPARCL1knockoutsproutsshowanalteredvesselstructurecomparedtowildtypeinthemetatarsalexvivoangiogenesisassay.

• SPARCL1 interacts with endoglin as a potentialreceptortomediateitsanti-angiogeniceffects.


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IVBM2018

W048

iNOS mediated oxidative stress induces lym-phatic dysfunction during obesity

Sonia Rehal1, Raghu Kataru1,CatherineLy1,BabakMehrara1

1Memorial Sloan Kettering Cancer Center, New York, United States

• Inflammatory iNOSmediates lymphaticdysfunc-tioninobesemiceviaincreasednitrosativestress

• iNOS mediates lymphatic dysfunction via endo-thelialcelltoxicityandimpairedfunctionaloutput

• Lymphaticdysfunctioncanindependentlyinduceaninsulinresistanceresponse,suggestingitsroleinobesityrelatedpathology

W049

High salt diet results in enhanced lymph flow in the skin of rats

Tore Reikvam1,2, Tine Veronica Karlsen1,ElhamNikpey1, Olav Tenstad1,HelgeWiig1

1University Of Bergen, Bergen, Norway, 2Norwegian Health Association, , Norway

• Skinserveasasodiumreservoirandcontributeinsodium homeostasis

• Rats given high salt had higher blood pressurethanthoseonlowsaltdiet

• Highsaltdietenhanceslymphflowandincreasesinterstitialfluiddrainagefromtheskinofrats.

W050

Desert Hedgehog promotes endothelium integrity through Smoothened dependent and independent pathways

SarahGuimbal1,Pierre-LouisHollier1, Caroline Caradu1, AnnabelReynaud1,Alain-PierreGadeau1, Marie-Ange Renault1

1Inserm U1034, Pessac, France

• Endothelium-derived Desert Hedgehog promotes VE-Cadherin-dependent junction integrity viaSmoothened

• Endothelium-derived Desert Hedgehog inhib-its VCAM-1 expression independently onSmoothened

• Smoothened AGonist (SAG) promotes VE-Cad-herin-dependent junction integritybutdoesnotlimitendothelialcellactivation

W051

Loss of Dhx15 gene expression causes vas-cular alterations and impairs endothelial cell energy metabolism

Jordi Ribera1,BernatCórdoba1,IrenePortolés1, Esther Fernández1,BernardinoGonzalez-de-la-Presa1,WladimiroJimenez1,2,WilliamC.Sessa3, Manuel Morales-Ruiz1,2

1Biochemistry and Molecular Genetics Department, Hospital Clínic of Barcelona, Institut d’Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Barcelona, Spain, 2Department of Biomedicine-Biochemistry Unit, School of Medicine, University of Barcelona, Barcelona, Spain, 3Vascular Biology and Therapeutics Program, Department of Pharmacology, Yale University, School of Medicine, New Haven, USA

• Homozygous loss of Dhx15 gene shows a lethalphenotypeinembryos.

• Dhx15+/-miceshowdiminishedbloodand lym-phaticvasculardensity.

• Silencing of Dhx15 gene expression in mouseendothelial cells is associated with alterationsin carbohydratemetabolism and cellular energyproduction.

W052

Identification of permeability permissive ves-sels and their molecular markers using correl-ative intravital imaging

Mark Richards1, Naoki Honkura1,BarbaraLaviña1, Miguel Sáinz-Jaspeado1, Christer Betsholtz1,LenaClaesson-Welsh1

1Dept. Immunology, Genetics and Pathology, Uppsala, Sweden

• Vascularpermeabilitycanbereproduciblyvisual-isedusingintravitalimagingandmicroinjection.

• Permeabilitypermissivevesselsandspecificsitesofvesselleakageremainlargelyconsistent.

• Claudin5,butnotothertightjunctionproteins,isa vital determinant of vessel leakage.

W053

Isoflurane anesthesia reduces calcium activity in mouse brain endothelial cells in vivo.

LingyanShi1, Adrian Rodriguez-contreras1

1City University Of New York, New York, United States, 2Columbia University, New York, United States

• Spontaneouscalciumtransientscanbemeasuredinawakemiceexpressingcytoplasmicandmem-branetargetedGCaMP6inbrainendothelialcells.

• Spontaneous calcium transients do not correlate withvasodilationevents.

• Isoflurane,aknownvasodilator,reducesthefre-quency and amplitude of calcium transients inbrainendothelialcells.


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IVBM2018

W054

Aflibercept-mediated morpho-functional recovery of the ischemic murine retina

Jose Eduardo Rojo Arias1,MatinaEconomopoulou2, HenningMorawietz3,RichardHWFunk1, Jozsef Jaszai1

1TU Dresden, Faculty of Medicine, Department of Anatomy, Dresden, Germany, 2TU Dresden, Department of Ophthalmology, Dresden, Germany, 3TU Dresden, Clinic III, Division of Vascular Endothelium and Microcirculation, Dresden, Germany

• AFL strongly inhibits neovascularization whilepromotingatip-celldrivenorderedrevasculariza-tionoftheischemicretinainOIRmice

• AFLreducesinflammatoryresponsesbydecreas-ing vasopermeability and shifting the activationstatusofmicroglia/macrophagesinOIRretina

• AFLimproveslightresponsivenessoftheretinainOIR mice in dose-dependent manner

W055

The role of actin regulation in the making of a blood vessel network

Andre Rosa1,2,3, Silvanus Alt1,2,3, Katja Meier1,2,3, Irene Holfinger1,2,3, Holger Gerhardt1,2,3

1Max Delbrück Center For Molecular Medicine In The Helmholtz Association, Berlin, Germany, 2DZHK (German Centre for Cardiovascular Research), partner site Berlin, Berlin, Germany, 3Berlin Institute of Health, Berlin, Germany

• Waspishighlyexpressedinsproutinganddevel-opingvascularnetworks

• WaspandArp2/3playacrucialruleduringendo-thelialcellmigration

• Waspisrequiredforcorrectarterial-venouscon-nectionsandvasculartone

W056

Loss of RGS5 in pericytes effects vascular repair after stroke

Michaela Roth1, Ilknur Özen1,ThomasPadel1, Guillem Genové2,GesinePaul1,3

1Translational Neurology Group, Department of Clinical Science, Wallenberg Neuroscience Center, Lund University, Lund, Sweden, 2Integrated Cardio Metabolic Center, Department of Medicine, Karolinska Institute, Huddinge, Sweden, 3Department of Neurology, Scania University Hospital, Lund, Sweden

• Regulator of G-protein signaling 5 (RGS5) loss in pericytes results in higher number of pericytesafterstroke

• LossofRGS5inpericytesleadstoincreasedvas-cular remodeling

• RGS5 loss in pericytes results in partial reduc-tioninBBBbreakdownandreducesinfiltrationofmonocytesafterstroke

W057

Lympedema / lipedema / obesity in clinical practice - differences and interconnection

Aleksandra Rovnaia1

1St Petersburg State Medical University, St Petersburg, Russian Federation

• Around50%patientswithlymphedemagoundi-agnosted or misdiagnosted, so do not recieve the right treatment

• Lymphedema, lipedemaandobesityarethedis-easeswhen thedifferentialdiagnosis inside thisgroupcanbecomplicated

• Lipedemaandmorbidobesitycanleadtolymph-edema onset and progressing

W058

SUR1-E1506K mutation impairs glucose tol-erance and promotes atherosclerotic plaque maturation in LDLR-/- mice

Anna-Kaisa Ruotsalainen1, Erika Gurzeler1, Anssi Laine1, Teemu Valkama1, Markku Laakso2,SeppoYlä-Herttuala1,3

1University Of Eastern Finland, A.I.Virtanen Institute for Molecular Sciences, Kuopio, Finland, 2Department of Medicine, University of Eastern Finland and Kuopio University Hospital, Kuopio, Finland, 3Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• E1506K mutation in the sulfonylurea receptorSUR1 induces glucose intolerance due a failure to increaseinsulincontentinLDLr-/-mice.

• SUR1-E1506KmarkedlyincreasedatheroscleroticplaquenecrosisandcalcificationinLDLr-/-mice.

• A novel mousemodel, wherein type 2 diabeticfactors promote atherosclerotic plaquematura-tion,leadingtounfavorableplaquephenotype.


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IVBM2018

W059

Flow-induced microRNAs prevent endothe-lial dysfunction and attenuate development of pulmonary hypertension in Sugen/hypoxia mice

HebahSindi1, Giusy Russomanno1, Claire Morgan1, VahithaAbdul-Salam1,AlexanderAinscough1, Beata Wojciak-Stothard1

1Imperial College of London, London, United Kingdom

• KLF2-induced exosomal miR-181 and miR-324attenuateapoptosisandinflammatoryresponsesinhumanpulmonaryendothelialcells.

• KLF2-induced miRs are reduced, and their gene targetsincreasedincellsfromIPAHpatientsandlungsfromPHmice.

• Therapeutic supplementation of miR-181 andmiR-324 attenuates development of pulmonaryhypertensioninSugen/hypoxiamice.

W060

Endothelium-protective and anti-remodelling effects of miR-150/PTPMT1 in pulmonary arterial hypertension

Giusy Russomanno1, Ahmed Osman1, Claire Morgan1, OlivierDubois1,VahithaAbdul-Salam1,BeataWojciak-Stothard1

1Imperial College of London, London, United Kingdom

• miR-150 reduced endothelial apoptosis, prolifer-ationandpro-inflammatoryactivationinvitrobydownregulating mitochondrial protein tyrosinephosphatasePTPMT1

• Endothelium-targeteddeliveryofmiR-150atten-uated development of pulmonary hypertensionanddownregulatedPTPMT1expression in lungsofpulmonaryhypertensivemice.

• Endothelial progenitor stem cells (EPSCs) fromidiopathicPAHpatientsshowedreducedmiR-150levelsandincreasedPTPMT1expression

W061

Susceptibility of LDL to aggregate predicts future cardiovascular deaths and is modifiable

Maija Ruuth1,2,SuDuyNguyen1, Terhi Vihervaara3, Mika Hilvo3, Teemu Daniel Laajala4,5,PradeepKumarKondadi6, Anton Gisterå7, Hanna Lähteenmäki1,TiiaKittilä1, Jenni Huusko8,MattiUusitupa9,UrsulaSchwab9,10, Markku Savolainen11, Juha Sinisalo12, Marja-Liisa Lokki13, Markku S Nieminen12,AnttiJula14,MarkusPerola14,15, Seppo Ylä-Herttuala8,16,LawrenceRudel17, Anssi Öörni18, Marc Baumann19, Amos Baruch20, Reijo Laaksonen3,21,22, Daniel FJ Ketelhuth7,TeroAittokallio4,5,MattiJauhiainen23,14, Reijo Käkelä24, Jan Borén6,KevinJonWilliams6,PetriKovanen1, Katariina Öörni1,24

1Wihuri Research Institute, Helsinki, Finland, 2Faculty of Medicine, Research Program Unit, University of Helsinki, Helsinki, Finland, 3Zora Biosciences, Espoo, Finland, 4Institute for Molecular Medicine Finland (FIMM), University of Helsinki, Helsinki, Finland, 5Department of Mathematics and Statistics, University of Turku, Turku, Finland, 6University of Gothenburg, Gothenburg, Sweden, 7Department of Medicine, Karolinska University Hospital, Karolinska Institute, Stockholm, Sweden, 8A.I.Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, 9School of Medicine, Institute of Public Health and Clinical Nutrition, University of Eastern Finland, , Finland, 10Institute of Clinical Medicine, Internal Medicine, Kuopio University Hospital, Kuopio, Finland, 11University of Oulu, Oulu, Finland, and Medical Research Center, Oulu University Hospital, Oulu, Finland, 12Heart and Lung Center, Helsinki University Hospital and University of Helsinki, Helsinki, Finland, 13Transplantation Laboratory, Medicum, University of Helsinki, Helsinki, Finland, 14Genomics and Biomarkers Unit, Department of Health, National Institute for Health and Welfare, Helsinki, Finland, 15Institute for Molecular Medicine Finland and Diabetes and Obesity Research Program, University of Helsinki, Helsinki, Finland, 16Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland, 17Wake Forest School of Medicine, Winston-Salem, USA, 18Åbo Akademi University, , Finland, 19Faculty of Medicine, Meilahti Clinical Proteomics Core Facility, University of Helsinki, Helsinki, Finland, 20Genentech Research and Early Development, South San Francisco, USA, 21Finnish Cardiovascular Research Center, University of Tampere, Tampere, Finland, 22Finnish Clinical Biobank Tampere, University Hospital of Tampere, Tampere, Finland, 23Minerva Foundation Institute for Medical Research, Helsinki, Finland, 24Faculty of Biological and Environmental Sciences, University of Helsinki, Helsinki, Finland

• This work identifies a key quality of LDL – itssusceptibility to aggregate– as anovelmeasur-ableandmodifiable factor in theprogressionofhumanatheroscleroticcardiovasculardisease.

• Aggregation-prone LDL predicts cardiovaculardeaths.

• Susceptibility of LDL particles to aggregate isreducedbyPCSK9inhibitorandbyhealthydiet.

• Aims


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IVBM2018

W062

FOXC1 is a major transcription factor in ath-erosclerotic plaques influencing SMC activa-tion

Urszula Rykaczewska1, Catarina Rippe2, Thomas Quertermous3,KarlSwärd2, Ulf Hedin1,LjubicaPerisicMatic1

1Department of Molecular Medicine and Surgery, Karolinska Institute, Stockholm, Sweden, 2Department of Experimental Medical Science, Lund University, Lund, Sweden, 3Division of Cardiovascular Medicine, Stanford University, Stanford, United States of America

• Combinedtranscriptomicandproteomicprofilingrevealed FOXC1 as a major transcription factorregulatingmoleculesdysregulatedinhumanath-eroscleroticplaques.

• InhealthyarteriesFOXC1associateswithsmoothmusclecellsandheparan-sulfatesynthesis,whileinlesionswiththyroidhormonebinding.

• FOXC1maybeinvolvedinSMCactivationinvas-cularinjuryandtherebyinfluenceatheroscleroticlesionprogressionandstability.

W063

Characterization of circular RNAs and microR-NAs in vascular calcification

Juhee Ryu1,2, Geon Jeong1,Yeong-HwanLim1,Duk-HwaKwon2,NakwonChoe2, Sera Shin2,HyunKook2,Young-KookKim1

1Department of Biochemistry, Chonnam National University Medical School, Hwasun, South Korea, 2Department of Pharmacology, Chonnam National University Medical School, Hwasun, South Korea

• CircRNAsareexpressedinvascularsmoothmus-clecellswithvascularcalcification

• CircRNAsregulatevascularcalcification• CircRNAs can act as miRNA sponges and may

havebiologicalfunctions

W064

Models for VEGF-B induced physiological and pathological cardiac hypertrophy

Markus Räsänen1, Karthik Hemanthakumar Amudhala1, JenniferPaech1,IbrahimSultan1, Deepak Ramanujam2, MariusRobciuc1, Johanna Lähteenvuo3, Stefan Engelhardt2, Riikka Kivelä1, Kari Alitalo1

1Wihuri Research Institute, Helsinki, Finland, 2Institut für Pharmakologie und Toxikologie, Technische Universität München, Munich, Germany, 3A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland

• Cardiomyocyte-specificoverexpressionofVEGF-Bleads to physiological, “athlete-like” cardiachypertrophy.

• ThesiteofexpressionofVEGF-Biscriticalforitseffects:autocrineendothelialoverexpressionviatheaP2promoterleadstopathologicalhypertro-phiccardiomyopathy.

• Comparison of the differences between phys-iological and pathological cardiac hypertrophyshouldrevealnewdruggabletargetsintheheart.

W065

Endothelial cell shape regulation by the scaf-fold protein Palmdelphin

Miguel Sainz-Jaspeado1, Ross Smith1, Naoki Honkura1, CansaranSaygili2,MichaelVanladewijck1, Christer Betsholtz1,TatianaPetrova2, Manfred Kilimann3, Lena Claesson-Welsh1

1Uppsala University, Department of Immunology, Genetics and Pathology, Rudbeck Laboratory, Science for Life Laboratory, Uppsala, Sweden, 2University of Lausanneand University of Lausanne Hospital, Department of Fundamental Oncology, Ludwig Institute for Cancer Research and Division of Experimental Pathology, Lausanne, Switzerland, 3Göttingen University Medical School, Department of Otolaryngology, Goettingen, Germany

• Endothelial cell and nuclear comunication andinteraction

• Cellshapeandnuclearmembraneintegity• Invitroandinvivostudyofendothelialcellshape

controlandorganization


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IVBM2018

W067

S100A4, a key player in plaque stabilization?

Antonija Sakic1, Mariam Grigorian2, Noona Ambartsumian2,Marie-LuceBochaton-Piallat1

1University of Geneva, Faculty of Medicine, Geneva, Switzerland, 2Institute of Cancer Biology, Danish Cancer Society , Copenhagen, Denmark

• Multimeric S100A4 and PDGF-BB act in synergyto induce a pro-inflammatory synthetic smoothmusclecellphenotype,likelythroughTLR-4.

• RNA sequencing showed strong upregulation ofpro-inflammatorygeneswhencellsweretreatedwithmultimericS100A4andPDGF-BBtogether.

• Our results suggest that the neutralization ofextracellular S100A4 decreases plaque size andpromotesplaquestabilization.

W068

Increased expression of complement compo-nents C2, C3 and C5 in patients with ascend-ing aortic aneurysm.

Tuija Huusko1, Katri Ruokamo-Korva1,PanuTaskinen3, Sakari Kakko1, Markku J Savolainen1,2, Tuire Salonurmi1,2

1Research Unit of Internal Medicine, Medical Research Center Oulu, Oulu University Hospital and University Of Oulu, Oulu, Finland, 2Biocenter Oulu, University of Oulu, Oulu, Finland, 3Department of Surgery, Oulu University Hospital and University of Oulu, Oulu, Finland

• Thereisanurgentneedforareliableearlydiag-nosticmethodfortheascendingaorticaneurysm(AscAA)

• OurresultsshowthatthecomplementcascadeisactivatedintheAscAAtissueandthealterationstakeplacebetweencomponentsC4andC7.

• Concentration of C3 was significantly higher intheplasmaofAscAApatients.

W069

The role of cortactin in leukocyte transmigra-tion into the central nervous system

Maryna Samus1,DietmarVestweber1

1Max Planck Institute for Molecular Biomedicine, Muenster, Germany

• Lack of cortactin results in reduced severity ofactiveEAE.

• CortactinisinvolvedintheregulationofvascularpermeabilitywithintheCNSbarriers.

• Absenceofcortactin leadstoreduced leukocyteinfiltration into the EAE-affected brain and thespinal cord.

W070

Anatomical distributions of vasa vasorum and lymphatic vasa vasorum in human aortic adventitia

Masaki Sano1

1Hamamatsu University School Of Medicine, 1-20-1 Handayama, Higashi-ku, Hamamatsu, Japan

• Asignificantcorrelationwas foundbetween thenumbersofVVandmedialthickness.

• Therewasnosignificantcorrelationbetweenthatof LVV and LVV distribution wasmost dense ininfra-renalabdominalaorta.

• Differences in the distributions of VV and LVVmayimplytheprevalenceofeachaorticdisease.

W071

Drug repositioning as an effective therapy for Protease-Activated Receptor-2 inhibition

Uzma Saqib1

1Indian Institute Of Technology, , India

W072

Ganglioside contributes to insulin resistance in senescent and TNFα-stimulated human aortic endothelial cells

Norihiko Sasaki1,YokoItakura1,MasashiToyoda1

1Department Of Geriatric Medicine (vascular Medicine), Tokyo Metropolitan Institute Of Gerontology, Sakaecho 35-2, Itabashi-ku, Japan

• Increased ganglioside in senescent endothelial cellscontributestoinsulinresistance.

• Theexpression levelsofgangliosidesaftertreat-ment with different concentrations of TNFα for differenttime intervalswereexamined inendo-thelial cells.

• Insulinsignalingandrelated-moleculesbyimmu-noblottingafterTNFαtreatmentwithorwithoutinhibitor of ganglioside synthesis was examinedin endothelial cells.


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IVBM2018

W073

OSGIN1 and OSGIN2 regulate adhesion of HCAEC and potentially contribute to endothe-lial erosion of plaques

Sandro Satta1

1Manchester Metropolitan University, Manchester, United Kingdom

• Endothelial erosion of atherosclerotic plaquestriggers about a third of heart attacks and iscausedbyendothelialcelldetachment.

• Ourinvitromodeloferosionidentifiedanupreg-ulationofOSGIN1andOSGIN2underconditionsof cells detachment.

• OSGIN1 and 2 overexpression induce detach-ment,dysregulateautophagyand induce senes-cenceinhumancoronaryarteryendothelialcells.

W074

Determining the protein atlas of normal and glioblastoma blood-brain barrier

J. B. Schaffenrath1, M. Neidert1, L. Regli1, A. Keller1

1Department of Neurosurgery, University Hospital Zürich, Zürich, Switzerland

• GBM vasculature shows deregulation of severalSLC transporters compared to normal human brainvasculature.

• Expression of the majority of ABC transportersremains unaltered in GBM vasculature.

• However, expression of P-glycoprotein is down-regulated on GBM vasculature.

W075

Following up the growth of blood vessels in a new in vivo wound healing model

Martin Schneider1

1Eth Zurich, Zurich, Switzerland

• Newinvivowoundhealingmodel• Very high temporal- and spatial resolution of

bloodvesselgrowth• nfluencing the angiogenesis process with tar-

getedtherapies:sunitinib

W076

Tight junction adapter protein cingulin regu-lates vascular barrier function in vivo

Klaudia Schossleitner1,KristinaZhuravleva2, Silvio Holzner1, Ole Goertz2,PeterPetzelbauer1

1Skin and Endothelium Research Division, Department of Dermatology, Medical University Vienna, Vienna, Austria, 2Department of Plastic and Hand Surgery, Burn Center, BG-University Hospital Bergmannsheil, Ruhr University Bochum, Bochum, Germany

• Tightjunctionadapterproteincingulinispresentin vascular endothelial cells

• Cingulinisdifferentiallyexpressedinhumanskin,lungandbrainendothelialcells

• Cingulin regulates endothelial permeability inmouse models of vascular leak

W077

Targeting smooth muscle cell TGF-β super-family pathways in vein graft neointima forma-tion

Julian Tristan Schwartze1,SammyEl-Mansi1,DanielKelly1, EmmaLouiseLow1, Menzo Havenga2,StuartAnthonyNicklin1,AndrewBaker3,AngelaCatherineBradshaw1

1Institute for Cardiovascular and Medical Sciences, University Of Glasgow, Glasgow, United Kingdom, 2Batavia Biosciences, B.V., Leiden, Netherlands, 3Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom

• Activin-like kinase (ALK)5 and ALK1 receptorsarepresentinpre-implantationsaphenousveins(SVs) from coronary artery bypass graft (CABG)patients

• Transforminggrowthfactor(TGF)-β1/ALK5signal-linginducescontractileSMCmarkerexpressioninSVSMCsfromCABGpatients

• Bone morphogenetic protein-9 antagonisesTGF-β1/ALK5-mediated increase in angiotensinII-induced intracellular Ca2+ release, identifyingpotentialtargetstoenhanceafavourableSVSMCphenotype


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IVBM2018

W078

The role of CD99 and CD99L2 in neutrophil diapedesis through the blood vessel wall

Kerstin Schäfer1, Silke Currie1,StefanVolkery1,LydiaSorokin2,DietmarVestweber1

1Max-Planck-Institut Münster, Münster, Germany, 2Institute of Physiological Chemistry and Pathobiochemistry, Münster, Germany

• CD99 KO mice show an adhesion and transmi-grationdefect. Leukocytes get trappedbetweenendothelialcellsandbasementmembrane.

• CD99L2 KO mice show a transmigration defectbutnoadhesiondefect.

• Establishment of visualization of the migrationof neutrophils by confocal intravital microscopy(IVM).

W079

Familial brain arteriovenous malformations: detection of novel candidate loci by Whole Exome Sequencing analysis

Concetta Scimone1,2, Luigi Donato1,2,3, Sara Guido1, Simona Alibrandi1, Carmela Rinaldi1, Rosalia D’Angelo1, Antonina Sidoti1,2

1Department of Biomedical and Dental Science and of Morphological and Functional Images, University of Messina, Messina, Italy, 2Department of Vanguard Medicine and Therapies, Biomolecular Strategies and Neuroscience, I.E.ME.S.T., Palermo, Italy, 3Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy

• Novelbrainarteriovenousmalformationsassoci-ated loci

• Rarecaseoffamilialarteriovenousmalformationofthebrainwithouthereditaryhaemorrhagictel-angiectasia

• Contributionofnextgenerationsequencingtech-nologyforgeneticcomplexdiseases

W081

In vivo dynamics and targeting of vessel co-option in glioblastoma

Giorgio Seano1,2, Amelie Griveau3, Samuel J. Shelton3, Shanmugarajan Krishnan2,RobertKupp4, Arman Jahangiri3, KirstenObernier3,OlleR.Lindberg3,TracyJ.Yuen3, An-Chi Tien3,JenniferK.Sabo3,NancyWang2,IvyChen2, Jonas Kloepper2,LouisLarrouquere2, Mitrajit Ghosh2,ItayTirosh5, Emmanuelle Huillard6,ArturoAlvarez-Buylla3, Michael C. Oldham3,AndersI.Persson3,WilliamA.Weiss3, TracyT.Batchelor2, Anat Stemmer- Rachamimov2, Mario L. Suva2,JoannaJ.Phillips3, Manish K. Aghi3,ShwetalMehta4, Rakesh K. Jain2,DavidH.Rowitch3

1Institut Curie Research Center, Orsay-Paris, France, 2Massachusetts General Hospital, Harvard Medical School, Boston, USA, 3University of California San Francisco, San Francisco, USA, 4Saint Joseph’s Hospital and Medical Center, Phoenix, USA, 5Broad Institute of Harvard and MIT, Cambridge, USA, 6ICM Brain and Spine Institute, Paris, France

• Olig2+ glioma cells invade by single-cell vesselco-option and preserve the blood-brain-barrier(BBB),whileOlig2-negativecellsformdenseperi-vascular collections, promote angiogenesis andBBBbreakdown.

• Wnt7 deletion or pharmacologicWnt inhibitionblocksOlig2+glioma single-cell vessel co-optionand enhances responses to temozolomide.

• Angiogenesisandvesselco-optionarealternativeand resistant mechanisms to reach vasculature

W082

Endothelial Dab1 Signaling Orchestrates Neu-ro-glia-vessel Communication in the CNS

Marta Segarra1,MariaR.Aburto1,2, Florian Cop1,CecíliaLlaó-Cid1, Ricarda Haertl1, Miriam Damm1,2, Ioanna Bethani1,MartaParrilla4, Anne Schaenzer3, Hannah Schlierbach3, Till Acker3, Laura Mohr1,MathiasRitter1, AmparoAcker-Palmer1,2,4

1Buchmann Institute for Molecular Life Science, Goethe University Frankfurt, Frankfurt am Main, Germany, 2Focus Program Translational Neurosciences (FTN), University of Mainz, Mainz, Germany, 3Institute of Neuropathology, University of Giessen, Giessen, Germany, 4Max Planck Institute for Brain Research, Frankfurt am Main, Germany

• CNSvascularisation• Blood-brainbarrier• Corticogenesis


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IVBM2018

W083

Tissue hypoxia induces the mobilisation from the spleen of pro-angiogenic neutrophils through sympathetic nerves activation.

Cédric Seignez1,MiaPhillipson1

1Dept. of Medical Cell Biology, Biomedical Center, Uppsala University, , Sweden

• Neutrophils display a specific subpopulation(CD49d+ VEGFR1+ CXCR4high MMP9high) withpro-angiogenicproperties.

• Pro-angiogenic neutrophils are stored in thespleen fromwhere theyarepromptlymobilisedbytheactivationofsympatheticnerves.

• Pro-angiogenic neutrophils are recruited intoVEGF-A- and CXCL12-producing hypoxic tissuesthrough the engagement of the integrin CD49d.

W084

Correlation of Computed Tomography with Carotid Plaque Transcriptomes Associates Calcification to Lesion-Stabilization

Eva Karlöf1,2, Till Seime2, Nuno Dias3,MarietteLengquist2, AnnaWitasp4,HåkanAlmquist5,JacobOdeberg6, Lars Maegdefessel7,8,PeterStenvinkel4,LjubicaPerisicMatic2, Ulf Hedin1,2

1Department of Vascular Surgery, Karolinska University Hospital, Stockholm, Sweden, 2Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden, 3Department of Angiology, Skåne University Hospital, Malmö, Sweden, 4Division of Renal Medicine, Department of Clinical Sciences, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden, 5Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden, 6Science for Life Laboratory, Department of Proteomics, School of Biotechnology, Royal Institute of Technology, Stockholm, Sweden, 7Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University Munich, Munich, Germany, 8Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden

• Correlation of preoperative CT analysis andcarotidplaque transcriptomes reveales an asso-ciation between macro calcification and geneexpressionprofilesrelatedtoplaquestability.

• Highlycalcifiedlesionscorrelatewithanincreasein SMC contractility markers, collagenous ECMcompositionandrepressedinflammation.

• PRG4,previouslyundescribed inatherosclerosis,is enriched in the ECMof calcified plaques andrelated to osteo-chondrogenesis.

W085

Effect of activation of purinoreceptor signal-ling on endothelial dysfunction

Anna Selmi1,HalszkaPonamarczuk1, Anna Gdula1, Marcin Popielarski1,MariaŚwiątkowska1

1Department of Cytobiology and Proteomics,Medical University of Lodz, Lodz, Poland

• During our study the effect of ADP-receptor’santagonistsincombinationwithagonistsofade-nosinereceptorsonendothelialdysfunctionwasanalyzed.

• Markersofendothelialdysfunctionwerecheckedin inflammatory stimulated and non-stimulatedendothelial cells.

• Presentedwork elucidate the effect onAR ago-nistsonmodulationofinflammatoryresponseinendothelial cells.

W086

Interpreting genetic variation in Coronary Artery Disease (CAD)

Ilakya Selvarajan1, Anu Toropainen1, Markku Laakso2, MinnaKaikkonen-Määttä1

1A. I. Virtanen Institute, University Of Eastern Finland, Kuopio, Finland, 2Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland

• WeaimtofunctionallycharacterizeofSNPsasso-ciatedwithCADbyfocusingoursearchforcausalSNPstoenhancersofthedisease.

• We usedHi-C, regression analysis and eQTLs toidentifyassociatedtargetgenes.

• Weperformed reporter assay to investigate theability of the causal regulatory SNPs to alterexpressioninanallele-specificway.


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IVBM2018

W087

Interplay between substrate stiffness, pro-an-giogenic cues and adhesion ligands for regu-lating endothelial cell force exertion

Apeksha Shapeti1,AliciaIzquierdo-Alvarez1, Diego A Vargas1,AlvaroJorge-Peñas1,HansVanOosterwyck1,2

1Biomechanics Section, Department of Mechanical Engineering, KU Leuven, Leuven, Belgium, 2Prometheus, Division of Skeletal Tissue Engineering, KU Leuven, Leuven, Belgium

• Cellular tractions were calculated by means oftractionforcemicroscopyonpolyacrylamide(PA)substrateswithvaryingstiffnessesandadhesionligands

• Chemical cues and PA stiffness increased totalforce exertion in an adhesion ligand dependentmanner

• Differences in total cellular force trends fromvaryingadhesionligandscouldbeexplainedfromthe characterizationof subcellular peak tractionareas

W088

Role of RGS5 in pulmonary vascular homeo-stasis

Neha Sharma1, Chandran Nagaraj2,BenceMiklosNagy2, DavorSkofic-Maurer3,GrazynaKwapiszewska2,3, Andrea Olschewski2,3,HorstOlschewski1,2

1Division of Pulmonology, Department of Internal Medicine, Medical University of Graz, Graz, Austria, 2Ludwig Boltzmann Institute for Lung Vascular Research, Graz, Austria, 3Otto Loewi Research Center, Medical University of Graz, Graz, Austria

• Role of Regulator of G protein signaling 5 (RGS5) isstillunknowninpulmonaryvasculature,

• RGS5 isupregulated inpulmonaryarteries frompulmonary hypertension associated with idio-pathic pulmonary fibrosis compared to healthycontrols,

• RGS5 Knockout mice has attenuated vasocon-strictive responseuponhighextracellularpotas-sium and serotonin

W089

FoxO-regulated endothelial stromelysin-1 pro-motes vascular injury and exudative phase of acute respiratory distress syndrome

Somanath P.R. Shenoy1, Sandeep Artham1, Fei Gao1

1Clinical and Experimental Therapeutics, College of Pharmacy, University of Georgia, Augusta, United States

• The study reports a novel role of endothelialFoxO-regulated stromelysin-1 expression in pul-monaryedemaandalveolarvascularinjury.

• Targeting FoxO1/3a using AS1842856 and stro-melysin-1 usingUK356618 for acute respiratorydistresssyndromeappearspromising.

• The study identifies stromelysin-1 analysis inbodyfluidsasasuitablebiomarkerforlunginjury.

W090

Endogenous anti-angiogenic factor sFlt-1/sVEGFR-1 is a possible inducer of preeclamp-sia

Masabumi Shibuya1,TadashiSasagawa1,YukikoMisawa1, Takeshi Nagamatsu2,TomoyukiFujii2,NobukoMimura2, Kazuki Morita2

1Jobu University, Takasaki, Japan, 2Dept. Obstetrics Gynecol., Univ. of Tokyo, Tokyo, Japan

• The sFlt-1, an endogenous anti-angiogenic fac-tor,isimportanttoinducepreeclampsia(PE).Wedeveloped a simpler ELISA to detect sFlt-1.

• Usingthisassay,wefoundthatPEserumcontainsabout4.7foldmoresFlt-1.comparedwiththoseinnormalpregnancy.

• Usingprimarytrophoblasts,wefoundthataHIFfamilymember isdeeply involved in sFlt-1geneexpressionathypoxia.


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IVBM2018

W091

Age-associated miRNAs expression induces senescence of microvascular endothelial cell via downregulation of HMGB2

Jae-Hoon Jeong1,2,HyeRamJo1,2, Young-Joo Shin3

1Korea Institute of Radiological & Medical Science, Seoul, South Korea, 2Korea University of Science and Technology, Daejeon, South Korea, 3Inje University Sanggye Paik Hospital, Seoul, South Korea

• HMGB2expressionwasdecreasedinoldhumanlung microvascular endothelial cells (HLMVECs) compared to young HLMVECs at transcriptionallevel.

• HMGB2geneknock-downinyoungHLMVECsledto inefficient DNA damage repair, decrease ofproliferationandlossofangiogenicfunction.

• MicroRNAs inducedwith age in HLMVECs,miR-217andmiR-181b-5p,downregulated the intra-cellular HMGB2 level and accelerated senes-cence.

W092

Robo4 and its novel binding protein TRAF7 suppress vascular hyperpermeability in inflammation.

Keisuke Shirakura1,RyosukeIshiba1, Taito Kashio1, Risa Funatsu1,WilliamC.Aird2, Takefumi Doi1,YoshiakiOkada1

1Osaka University, Suita, Japan, 2Beth israel Deaconess Med. Ctr, Boston, USA

• DepletionofRobo4increasedmortalityandvas-cularleakageinendotoxemicmice.

• TheC-terminusofRobo4 interactedwithTRAF7and suppressed TNFα-inducedendothelialhyper-permeability.

• Robo4andTRAF7suppressedendothelialhyper-permeability by stabilizing VE-Cadherin localiza-tion.

W093

Endothelial cell fitness dictates the source of regenerating liver vasculature

Mahak Singhal1,2,3,XiaotingLiu4,5, Donato Inverso1, Kai Jiang4, Jianing Dai4, Hao He4,5, Susanne Bartels1,WeipingLi5,6,AshikAhmedAbdulPari1,2,3,NicolasGengenbacher1,3, Eva Besemfelder1, Lijian Hui6,HellmutG.Augustin1,2,7, Junhao Hu4

1Division of Vascular Oncology and Metastasis Research, German Cancer Research Center Heidelberg (DKFZ-ZMBH Alliance), Heidelberg, Germany, 2Department of Vascular Biology and Tumor Angiogenesis, European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, 3Faculty of Biosciences, Heidelberg University, Heidelberg, Germany, 4Interdisciplinary Research Center on Biology and Chemistry, Shanghai Institute of Organic Chemistry, Chinese Academy of Sciences, Shanghai, China, 5University of Chinese Academy of Sciences, Beijing, Beijing, China, 6State Key Laboratory of Cell Biology, CAS Center for Excellence in Molecular Cell Science, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China, 7German Cancer Consortium, Heidelberg, Germany

• IrradiationcausedDNAdamage in resident liverEC,thusrequiringanemergencymobilizationandengraftmentofbonemarrow-derivedcells.

• Undernon-vascular-damaging conditioned,neo-vascularization proceeded exclusively by localexpansionofdifferentiatedEC.

• Stem cell-based regenerative therapies failed tocontribute to theneovascularizationof the liverwithhealthyremainingvessels.

W094

Preventing eNOS phosphorylation on Tyr657 attenuates endothelial dysfunction and car-diovascular disease through inhibition of PKM2

Mauro Siragusa1,2, Janina Thöle1,2,IrisS.Bibli1,2, Bert Luck1,2, Annemarieke E. Loot1, Kevin de Silva1,IlkaWittig2,3, Juliana Heidler2,3,VoahanginirinaRandriamboavonjy1,2, Karin Kohlstedt1, Bernhard Brüne4,AndreasWeigert4, Beate Fisslthaler1,2, Ingrid Fleming1,2

1Institute for Vascular Signalling, Goethe University, Frankfurt am Main, Germany, 2German Center for Cardiovascular Research (DZHK), Partner site RheinMain, Frankfurt am Main, Germany, 3Functional Proteomics, SFB 815 Core Unit, Goethe University, Frankfurt am Main, Germany, 4Institute of Biochemistry I, Goethe University, Frankfurt am Main, Germany

• ThephosphorylationofeNOSonTyr657isassoci-atedwithendothelialdysfunctionandcardiovas-cular disease development in vivo.

• S-nitrosation of PKM2 inhibits pyruvate kinaseactivity,resultingintheaccumulationofreducingequivalentsandattenuatednitrosativestress.

• Preserving NO bioavailability and signaling isimportant for the maintenance of endothelial redoxhomeostasis.


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W095

The role of the Y1173 phosphosite in VEGFR2 signaling

Elin Sjöberg1,MasabumiShibuya2,LenaClaesson-Welsh1

1Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 2Department of Molecular Oncology, Tokyo Medical and Dental University, Tokyo, Japan

• ThefivemajorVegfr2phosphositesY949,Y1052,Y1057,Y1173andY1212regulatespecificdown-streampathways.

• MassspectrometryidentifiesinteractionpartnersoftheY1173phosphosite.

• An inducible Vegfr2 (fl/Y1173F) mouse strainallowsus tostudytheeffectofpY1173removalonendothelialcellbiology

W096

The role of the Ca2+-activated Cl- channel TMEM16A in the pulmonary vasculature

Davor Skofic-Maurer1, Chandran Nagaraj2, Diana Zabini1,2, Neha Sharma3,GrazynaKwapiszewska1,2, Andrea Olschewski1,2

1Otto Loewi Research Center, Medical University of Graz, Graz, Austria, 2Ludwig Boltzmann Institute for Lung Vascular Research, , Austria, 3Department of Internal Medicine, Division of Pulmonology, Medical University of Graz, , Austria

• TheroleofTMEM16Aintheinthepulmonarycir-culationislargelyunknown.

• Overexpression of TMEM16A depolarizes therestingmembranepotentialofPAECandPASMC.

• IncreasedTMEM16Aexpressionlowerstheprolif-erationofPAECandaugmentstheproliferationofPASMCwhiletheapoptosisremainsunaffected.

W097

Vitamin C deficiency impairs ETB recep-tor-mediated vasoconstriction in uterine arter-ies undergoing remodeling

Gry Freja Skovsted1,PernilleTveden-Nyborg1, Jens Lykkesfeldt1

1Experimental Animal Models, Department of Veterinary and Animal Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, DK-1870 Frederiksberg C, Denmark, Frederiksberg, Denmark

• Endothelin type B receptors (ETBR) are upregu-lated in smooth muscle cells in uterine arteries duringpregnancy-inducedremodeling

• Vitamin C deficiency attenuates ETBR upregula-tionduringuterinearteryremodeling

• PoorvitCstatusaffectsuterinearteryremodelingduringpregnancy

W098

MicroRNA-532-5p regulates pericyte func-tion by targeting the transcription regulator BACH1 and Angiopoietin-1

Sadie Slater1, Eva Jover1, Andrea Martello2, Iker Rodriguez-Arabaolaza1, Rosa Vono3, Miss Valeria Alvino1, Simon Satchell1,GaiaSpinetti3, Andrea Caporali2,PaoloMadeddu1

1University of Bristol, Bristol, United Kingdom, 2Edinburgh University , Edinburgh, United Kingdom, 3IRCCS MultiMedica, Milan, Italy

• The secretory profile of vascular cells is keyin mediating angiogenesis, yet little is knownregarding regulation of angiogenic factors bypericytemicroRNAs.

• We investigated the expression of pericytemicroRNAsinresponsetohypoxia.

• We demonstrate a novel pro-angiogenic axis,withmiR-532-5pplayingapivotal role inmodu-latingpericyteangiopoietin-1expressionvia thetranscriptionfactorBACH1.

W099

Thymosin β4 regulates smooth muscle cell TGFβ/PDGF-BB signalling and mediates vas-cular protection via LRP1

SonaliMunshaw1, Susann Bruche1, Andia N. Redpath1, JyotiPatel1,KarinaN.Dubé1, Keith M. Channon1, Nicola Smart1

1University Of Oxford, Oxford, United Kingdom

• LRP1isanendocyticregulatorofTGFβ/PDGF-BBsignalling, which protects against aortic diseasebymaintainingstable,contractileVSMCs.

• We demonstrated an interaction between LRP1and Tβ4 and characterised aortic VSMC/elastindefects in Tβ4KOmice,whichpredisposetodis-ease.

• Tβ4-controlled endocytosis of LRP1 modulatesVSMCgrowthfactorresponses,identifyingTβ4 as apotentialtreatmentforvasculardisease.


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W100

Pulmonary endothelial dysfunction precedes formation of pulmonary metastases in breast cancer-bearing mice

Marta Smeda1, Anna Kieronska1, Mateusz Adamski1, BartoszProniewski1, Magdalena Sternak1, Tasnim Mohaissen1,KamilPrzyborowski1,KatarzynaDerszniak1, DawidKaczor1, Marta Stojak1,ElzbietaBuczek1, Agnieszka Jasztal1,JoannaWietrzyk2, Stefan Chlopicki1,3

1Jagiellonian University, Jagiellonian Centre for Experimental Therapeutics, Krakow, Poland, 2Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland, 3Jagiellonian University, Medical College, Krakow, Poland

• BreastcancermetastasisisassociatedwithearlypulmonaryendothelialdysfunctionevidencedbycompromisedNOproduction

• Atthetimeofmetastasisformationinthelungs,pulmonary endotheliumbecomes activated anditsbarrierfunctionislost

• Presenceoffirstmetastaticnodules inthe lungscoincidewiththephenotypeofEndMT

W101

Quantification of polymorphic sEng molecules using a new sandwich-ELISA system

Ilya Smirnov1,IrinaGryazeva1, Margarita Vasileva2, Irina Krutetskaia1, Olga Shashkova1,MarinaSamoylovich1, AnastasiaStolbovaya1,NellyaSolodovnikova2, Irina Zazerskaya2,DmitriySokolov3,SergeySelkov3, Vladimir Klimovich1

1Russian Research Center For Radiology And Surgical Technologies, Sain-Petersburg, Russian Federation, 2Almazov National Medical Research Center, Sain-Petersburg, Russian Federation, 3The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott, Sain-Petersburg, Russian Federation

• Different sandwich-ELISA systemsdetect variousamountsofsolubleendolgin.

• Antigenpolymorphismisthoughttobethemostlikely explanation of the differences in antigencontentestimations.

• AnELISA systemdetecting thehighest sEng lev-elswasvalidatedasaquick,specific,andpreciseinstrument.

W102

VEGFR2 pY1212 signaling regulates the Myc pathway and endothelial cell proliferation in a strain-dependent manner

ChiaraTestini1, Ross Smith1,YiJin1, Mats Hellström1, MasabumiShibuya2,LenaClaesson-Welsh1

1Uppsala University Department of Immunology, Genetics and Pathology, Uppsala, Sweden, 2Jobu University Institute of Physiology and Medicine, Takasaki, Japan

• In endothelial cells, Grb2 and PI3Kp85 binddirectly to pY1212/pY1214 of VEGFR2, whichcontributestodownstreamsignalingviaAKTandERK1/2.

• LossinAKTandERK1/2signalinginVegfr2Y1212F/Y1212Fmice impairMycpathway inductioninastrain-specificmanner resulting instrain-specificvascularphenotypesinmice.

• Signaling through VEGFR2 pY1212 regulates ECproliferationviainductionofMyc.

W103

Histone methyltransferase EZH2 inhibits hyal-uronan synthesis and impairs the glomerular endothelial glycocalyx in diabetic nephropa-thy

Marloes Sol1, Jiedong Qiu2, Johan van der Vlag3,Jacobvanden Born4,BenitoYard2,Jan-LuukHillebrands1, Jan Kamps1, Guido Krenning1

1Dept. of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, Netherlands, 2Dept. of Nephrology, Endocrinology and Rheumatology, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, 3Dept. of Nephrology, Radboud University Medical Center Nijmegen, Nijmegen, The Netherlands, 4Dept. Internal Medicine, Division Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands

• Indiabeticnephropathy,theglomerularendothe-lialglycocalyx is impaired, leadingtoproteinuriaandkidneyfailure.

• EZH2-mediated H3K27me3 is increased in glo-merularendothelialcellsindiabeticnephropathyandcorrelatedwithseverityofproteinuria.

• SilencingofEZH2invitroshowedupregulationofhyaluronan synthesis-enzymes, suggesting thatEZH2-mediatedH3K27me3reducesglycocalyxbyreducinghyaluronan.


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W104

Endothelial Cell Activation Is Regulated by Epidermal Growth Factor-Like Domain 7 (EGFL7) During Inflammation

SébastienPinte1, Bertrand Caetano1,AlexandraleBras1, Chantal Havet1, Gaëlle Villain1, Catherine Duez2, Virginie Mattot1, Fabrice Soncin1

1CNRS UMR8161, Institut Pasteur de Lille, Univ Lille, Lille, France, 2INSERM U1019, CNRS UMR 8204, Institut Pasteur de Lille, Univ Lille, Lille, France

• Egfl7 is down-regulated during inflammation invivo

• Egfl7 is regulated by inflammatory cytokines inendothelial cells

• Egfl7 regulates leukocyte adhesion receptors inendothelial cells

• Egfl7regulates theNFkBpathway inendothelialcells

W105

Integrated omics data analysis for new insights into the role of EZH2 in vascular biol-ogy

Iguaracy Sousa1,ChristianHauer2, Giovanni d’Ario2, Florian Nigsch2, José Krieger1

1Heart Institute - University of São Paulo, São Paulo, Brasil, 2Novartis Institute for Biomedical Research, Basel, Switzerland

• Integratingdifferentlayersofomicsdataallowedus to improve our understanding the EZH2’s role invascularbiology.

• We identified genes potentially regulated byEZH2 that have important roles in vascular integ-rity,celladhesion,andcellcommunication.

• Also,genesrelatedtocellcycleandcellprolifera-tion,relevanttothecontrolofangiogenesis.

W106

OLFML3 constitutes a new therapeutic target for colorectal carcinoma therapy

Jimmy Stalin1, Chiara Secondini2, Stephane Jemelin1, OrianaCoquoz2, Curzio Ruegg2, Beat Imhof1, Marijana Licina1

1Fribourg University, faculty of science and medecine, department of Oncology/Microbiology/Immunology, Fribourg, Switzerland, 2Geneva University, Centre medical universitaire, Department of Pathology and Immunology, Geneva, Switzerland

• Olfml3 is highly expressed on colorectal andbreastcancerbiopsiesandcouldbederegulatedbystandardofcaretherapies

• Olfml3 targeting decreases tumor growth andlymph/angiogenesisbutalsometastaticdissemi-nation inboth in-vivocolorectalandbreastcan-cer models

• Olfml3 targetingenhances infiltrationofanti-tu-morimmunecellspopulationincolorectalcancermodels and it increases anti-PD-1 therapeuticeffects

W107

PLVAP deletion in adult endothelium results in liver-independent protein calorie malnutrition and reduced survival

Sophie Deharvengt2, Nicole Smits3,AlisonYoung4, Radu Stan1,2,4

1Department of Biochemistry and Cell Biology, Geisel School of Medicine at Dartmouth, Lebanon, United States, 2Department of Pathology, Geisel School of Medicine at Dartmouth, Lebanon, United States, 3Department of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Lebanon, United States, 4Norris Cotton Caner Center, Geisel School of Medicine at Dartmouth, Lebanon, United States

• Inducible deletion of Plvap in adultmice (PlvapiECKO) results in loss of endothelial diaphragms, proteinlosingenteropathy,andreducedsurvival.

• ThephenotypesimilarbutlessseverethanwholeanimalPlvapdeletion

• Thephenotype isnotaresultof reducedfenes-traeporesnumbersinliversinusoids,asrecentlyproposed by work in independently generatedPLVAP-/-mice.


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W108

Plasmalemma vesicle associated protein (PLVAP) is a novel target for cancer immuno-therapy

Sophie J. Deharvengt2,PeishengZhang4,JacquelineY.Smith3,4, Catherine Carriere5, Chao Cheng6,MaryJoTurk4, Radu V. Stan1,2,3

1Department of Biochemistry and Cell Biology, Geisel School Of Medicine At Dartmouth, Lebanon, United States, 2Department of Pathology, Geisel School Of Medicine At Dartmouth, Lebanon, United States, 3Norris Cotton Cancer Center, Geisel School Of Medicine At Dartmouth, 4Department of Microbiology and Immunology, Geisel School Of Medicine At Dartmouth, 5Department of Medicine, Geisel School Of Medicine At Dartmouth, 6Department of Biomedical Data Science, Geisel School Of Medicine At Dartmouth,

• PLVAP is an endothelial specific protein highlyexpressed on the surface of tumor endothelialcells.

• Experiments by PLVAP gain of function, loss offunction and endothelial reconstitution providegenetic evidence that PLVAP facilitates tumorgrowth.

• EndothelialdeletionofPLVAPgeneorantagonismofPLVAPfunctioninhibittumorgrowthbyelicit-ingimmuneeffectoranti-tumorhostresponses.

W109

The shear stress-induced long non-coding RNA Lassie as a regulator of endothelial cell-cell junctions

Laura Stanicek1,2,DiewertjeBink1, Noelia Lozano-Vidal1, IlkaWittig3, Leo Kurian4,Hyouk-BumKwon5, Didier Stainier5, Alina Klems6,FerdinandleNoble6, Stefanie Dimmeler2,7, Reinier A. Boon1,2,7

1Department of Physiology, Institute for Cardiovascular Research, VU University Medical Center, Amsterdam, Netherlands, 2Institute of Cardiovascular Regeneration, Center of Molecular Medicine, Goethe-University , Frankfurt am Main, Germany, 3Functional Proteomics, SFB 815 Core Unity, Faculty of Medicine, Goethe-University , Frankfurt am Main, Germany, 4University of Cologne, Institute for Neurophysiology; Center for Molecular Medicine (CMMC) , Cologne, Germany, 5Max Planck Institute for Heart and Lung Research, Bad Nauheim , Germany, 6Department of Cell and Developmental Biology, KIT , Karlsruhe, Germany, 7German Center for Cardiovascular Research DZHK, Partner Site Frankfurt Rhine-Main, Berlin, Germany

• Thelongnon-codingRNALassieisupregulatedbyshearstressinhumansandzebrafish.

• Lassie is crucial for endothelial cell function assilencingimpairscellsurvivalandendothelialbar-rier.

• RNA pull-down and RNA immunoprecipitationexperimentsconfirmedseveral junctionproteins(e.g.PECAM-1andCaveolin-1)asLassie-interact-ing partners.

W110

PDGF-C / PDGFRα signaling in the patho-genic response following ischemic stroke

Manuel Zeitelhofer1, Milena Zeitelhofer Adzemovic1, Christina Stefanitsch1, Enming J Su2,SebastianALewandowski1, Lars Muhl1,DanielALawrence2, Ingrid Nilsson1, Linda Fredriksson1,2

1Karolinska Institutet, , Sweden, 2University of Michigan Medical School, Ann Arbor, USA

• PDGF-C/PDGFRαsignaling isakey regulatorofblood-brain barrier (BBB) function during isch-emic stroke

• The tyrosine kinase inhibitor imatinib influ-encesexpressionofgenes involved in forexam-ple immune cell diapedesis and preserves BBB integrityinaphotothromboticmodelofischemicstroke

W111

Endothelial Sodium Channel α (αENaC)-de-pendent regulation of endothelial function and endothelial barrier integrity

Magdalena Sternak1, Anna Bar1,2, Mateusz Grzegorz Adamski1, Tasnim Mohaissen1,3,BrygidaMarczyk1, Anna Kieronska1,2, Marta Stojak1, Kamil Kus1, Antoine Tarjus4, Frederic Jaisser4,5, Stefan Chlopicki1,2

1Jagiellonian Centre For Experimental Therapeutics (Jcet) Jagiellonian University, Krakow, Poland, 2Department of Pharmacology, Jagiellonian University Medical College, Krakow, Poland, 3Department of Toxicology, Jagiellonian University Medical College, Krakow, Poland, 4INSERM UMRS1138, Centre de Recherche des Cordeliers, Université Pierre et Marie Curie, Paris, France, 5INSERM, Clinical Investigation Centre 1433, Vandoeuvre-lès-Nancy, France

• In physiological conditions, endothelial αENaC contributestoAchandflow-inducedvasodilation

• In pathophysiological conditions endothelialαENaC contributes to the preservation of theendothelialbarrierfunction

• ThestimulationofendothelialαENaCmayaffordimprovedendothelialfunction


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W112

AMP-activated protein kinase alpha1 reg-ulates hexokinase to control proliferation during angiogenesis

Heike Stingl1,SvenZukunft1,RüdigerPopp1,VoahangyRandriamboavonjy,BeateFisslthaler1, Ingrid Fleming1

1Institute For Vascular Signalling, Frankfurt, Germany

• Endothelial AMPK alpha1 is crucial for retinalangiogenesisandendothelialcellproliferation.

• In vivo, tamoxifen-induced AMPK alpha1 defi-ciencycausesadownregulationofhexokinase1,whichaffectsendothelialproliferation.

• Thehexokinase1proteinisdownregulatedbyanincreased calpain activity in AMPK alpha1 defi-cient cells.

W113

Pharmacological modulation of metabolism by carbon monoxide and nitric oxide sup-press cancer-endothelial cells interactions

Marta Stojak1,PatrycjaKaczara1,RobertoMotterlini2, Stefan Chlopicki1

1Jagiellonian Centre for Experimental Therapeutics, Krakow, Poland, 2INSERM Unit 955, Equipe 12, Faculty of Medicine, University Paris-Est, Créteil, Paris, France

• CORM-401andPAPANONOate,givenaloneorincombination,modulate breast cancer cell adhe-sionandtransmigrationacrossthelungmicrovas-cular endothelium

• Theanti-adhesiveandanti-transmigratoryeffectsof CO and NO on cancer-endothelium inter-actions are linked with cellular bioenergeticschangesinbothcelllines

• Pharmacological attenuation of metabolism byCO-andNO-donorsrepresentanattractivetargetforpreventingofcancer-endothelialcellsinterac-tions

W114

Anti-endoglin monoclonal antibodies inhibit migration and endoglin shedding in endothe-lial cells EA.hy926

Anastasia Stolbovaya1,IlyaSmirnov1,IrinaGryaseva1, Irina Krutetskaia1,ProffesorMarinaSamoylovich1,DmitriySokolov2,ProffesorSergeySelkov2,ProffesorVladimirKlimovich1

1Russian Research Center For Radiology And Surgical Technologies named after ac. A.M. Granov, Saint-Petersburg, Russian Federation, 2The Research Institute of Obstetrics, Gynecology and Reproductology named after D.O. Ott, Saint-Petersburg, Russian Federation

• Monoclonalantibodiesagainstendoglinreducedendothelialcellmigrationinvitro

• It was shown for the first time that several ofanti-endoglinMABscouldinhibitCD105sheddingbyendothelialcells

• Monoclonalantibodiesagainstendoglincouldbeconsideredastoolforangiogenesisregulation

W116

Stem cell factor mediates pathological ocular angiogenesis

SongyiSeo1, Koung Li Kim1, Wonhee Suh1

1Chung-Ang University, seoul, South Korea

• TheexpressionlevelsofSCFandcKITincreaseinoculartissueswithpathologicalangiogenesis

• SCF/cKIT signaling promotes beta-catenin tran-scriptionalactivityathypoxia

• Blockade of SCF and cKIT inhibits pathologicalocular angiogenesis

W117

SIRT1 suppressed vascular smooth muscle cell senescence via phosphorylation of AMPK Ser-485

JinyoungSung1, Seul Gi Kim2,HyoungChulChoi3

1Department Of Pharmacology,College of Medicine, Yeungnam University, Daegu, South Korea, 2Department Of Pharmacology,College of Medicine, Yeungnam University, Daegu, South Korea, 3Department Of Pharmacology,College of Medicine, Yeungnam University, Daegu, South Korea

• Vascular senescence is associated with changesinthemechanicalandthestructuralpropertiesofthevascularwall,whichleadstothelossofarte-rialelasticityandreducedarterialcompliance.

• Our aim was to examine the role of SIRT1 andAMPK in VSMC senescence and to test howtheseproteinsfunctioninthecontextofcellularresponses to aging.


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W118

Targeted proteomics of endothelium-related proteins in murine model of metastatic breast cancer

Joanna Suraj1,2,AnnaKurpińska1,AgnieszkaZakrzewska1, Magdalena Sternak1, Marta Stojak1, Stefan Chlopicki1,3, MariaWalczak1,2

1Jagiellonian Centre For Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland, 2Chair and Department of Toxicology, Jagiellonian University Medical College, Krakow, Poland, 3Chair of Pharmacology, Jagiellonian University Medical College, Krakow, Poland

• Theearlyphaseofmetastasisinmouseplasmaisassociatedwithglycocalyxdisruption,endothelialinflammationand increased vascularpermeabil-ity.

• MicroLC/MS-MRMmethodenablestocharacter-izechangesinendothelialfunctioninbreastcan-cer development in mice.

• Multi-biomarkerapproachseemstobetheusefultool for mechanistic insight and comprehensiveunderstanding of early endothelial changes inmetastasis development.

W119

Expression Landscape of the Proprotein Con-vertase Subtilisin/Kexin (PCSK) Family in Vas-cular Disease

Bianca E. Suur1,MoritzLindquistLiljeqvist1,OttoBergman2,YuhuangLi2,3,MarietteLengquist1, Anton Razuvaev1,JacobOdeberg2,4,RobertDay5,GabiellePaulsson-Berne2, Göran K. Hansson2, Lars Maegdefessel2,3, PerEriksson2, Ulf Hedin1,JoyRoy1,LjubicaPerisicMatic1

1Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm, Sweden, 2Department of Medicine, Center for Molecular Medicine, Karolinska Institutet, Stockholm, Sweden, 3Department of Vascular and Endovascular Surgery, Klinikum rechts der Isar, Technical University Munich, Munich, Germany, 4Science for Life Laboratory, Department of Proteomics, School of Biotechnology, Royal Institute of Technology, Stockholm, Sweden, 5Sherbrooke University, Sherbrooke, Canada

• PCSK6wasthemostenrichedPCSKinatheroscle-rotic plaques and abdominal aneurysms. Furinupregulation was implicated in thoracic aneu-rysms.

• PCSK9 protein was abundant in atheroscleroticand aneurysm tissues, while mRNA expressionwas undetectable, suggesting its accumulationfromcirculation.

• PCSK5-9 correlatedwith clinical parameters andaneurysm biomechanics, which will be furtherexploredtoevaluatetheir riskpredictionpoten-tial.

W120

Modulation of the S1P/S1P receptor axis by an engineered S1P chaperone reduces vascu-lar reperfusion injury

Steven Swendeman1, Cecilia Frej1,YuHisano,TimothyHla1

1Boston Children’s Hospital, Boston, United States

• CreationofanS1Pchaperone,ApoM-Fc,tomod-ulateplasmaS1PlevelsinvivotointerrogatetheroleofS1Pinvascularreperfusioninjury

• ModulationofPlasmaS1P levelsusingApoM-Fcreduces hypertension and vascular reperfusioninjuryinvivo

• IdentificationofnovelApoM-dependentsignalingmechanisms in vitro

W121

Paraoxonase 1 lactonase activity in endothe-lial cells regulates vasodilation induced by arachidonic acid metabolite

Dan Gilad1,2,ShaharAtiya1,2, Ziv Mozes-Autmazgin1,2, RotemShellyBen-Shushan1,EytanAmram1,DimitryChuyun3, Andrea Szuchman-sapir1,2

1Laboratory of vascular signaling research, Migal-galilee Research Institute, , Israel, 2Tel-Hai college, Upper Galilee, Israel, 3The Baruch Padeh Medical Center, Poriya, Israel

• PON1penetratesendothelialcellsinthevascula-ture

• PON1 lactonase activity in the endotheliumaffectsvasculardilation

• PON1regulatiesCa2+influxmediatedbythelac-tone-containing EDHF 5,6-δ-DHTL.


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W122

BMP9 phenotypically alters the pulmonary microvascular endothelium in Pulmonary Arte-rial Hypertension

Robert Szulcek1, Nina Rol2,GonzaloSanchez-Duffhues1, XiaokePan2,ChrisDickhoff2,WimTimens3, Harm-Jan Bogaard2, Marie-José Goumans1

1Leiden University Medical Center, Leiden, Netherlands, 2VU Universtiy Medical Center, Amsterdam, Netherlands, 3University Medical Center Groningen, Groningen, Netherlands

• BMP9wastestedtoreinstateBoneMorphogenicProtein(BMP)signalinginpulmonaryendothelialcellsfromPulmonaryArterialHypertension(PAH)patients.

• BMP9restoredBMPreceptorlevelsinthemicro-vascular endothelium (MVEC) of PAH patients,butalsoactivatedTGFβ signaling.

• Repetitive BMP9 treatment induced phenotypicchangesinPAHMVEC,includinglossofjunctionalVE-cadherinandconsequentlydecreasedbarrierintegrity.

W123

Nanoparticle-Encapsulated Nucleoside-Mod-ified VEGFC mRNA (VEGFC mRNA-LNP) Induces Organ Specific Lymphatic Growth and Reverses Lymphedema

Dániel Imre Szőke1,2,AndreaStyevkónéDinnyés1,2, László Bálint1,2,GáborKovács1,2,KittiAjtay1,2,BarbaraL.Mui4, YingK.Tam4, Thomas D. Madden4, Katalin Karikó5,BabakJ. Mehrara6, Sagraria Ortega7, Michael J. Hope4,DrewWeissman3,NorbertPardi3, Zoltán Jakus1,2

1Department of Physiology, Semmelweis University School of Medicine, Budapest, Hungary, 2MTA-SE „Lendület” Lymphatic Physiology Research Group, Budapest, Hungary, 3University of Pennsylvania, Perelman School of Medicine, Philadelphia, USA, 4Acuitas Therapeutics, Vancouver, Canada, 5Biontech, Mainz, Germany, 6Department of Surgery, Division of Plastic and Reconstructive Surgery, Memorial Sloan Kettering Cancer Center, New York, USA, 7Transgenic Mice Core Unit, Spanish National Cancer Research Center, Madrid, Spain

• Wehavedevelopedanovelnanoparticle-encap-sulated nucleoside-modified codon-optimizedVEGFCmRNAsystem,whichisanovelapplicationofthemRNA-LNPplatform

• VEGFC mRNA-LNP complex administrationinduces organ specific lymphatic growth andactive lymphatic function in the newly formedlymphaticvessels

• VEGFC mRNA-LNP treatment reverses experi-mentallymphedema

W124

Clever-1 controls site-specific homing of lym-phocytes to the spleen

Sina Tadayon1, Johannes Dunkel1, Olga Halle2, Marika Karikoski1, Heidi Gerke1,PiaRantakari1,ReettaVirtakoivu1, OliverPabst3, Marko Salmi1, Maija Hollmén1, Sirpa Jalkanen1

1Turku University, Turku, Finland, 2Institute of Immunology, Hannover, Germany, 3Institute of Molecular Medicine, Aachen, Germany

• Red pulp is themajor site of lymphocyte entryinto the spleen

• Clever-1isexpressedexclusivelyonvesselsinthesplenic red pulp

• Clever-1 controls lymphocyte entry into thespleen

W125

Tetraspanin18 is a novel regulator of develop-mental and pathological angiogenesis.

Ikue Tai-Nagara1,YoshiakiKubota1

1Department of Anatomy, School of Medicine, Keio University, Shinjuku-ku, Japan

• Retinal vascular development, including radialgrowth and vertical sprouting, is suppressed inendothelialcell-specificTspan18KOmice.

• Tspan18knockoutmiceshownohemorrhage intransplanted tumor and decreased neovascular tuftareainROPmodel.

• Tspan18directlybinds toa fragmentofVEGFR2proteinandmayregulateVEGFR2signaling.

W126

A new type of lymphatic endothelial cells in the medulla of lymph nodes

Akira Takeda1,ImtiazIftakhar-E-Khuda1,MasayukiMiyasaka2, Sirpa Jalkanen1

1University of Turku, Turku, Finland, 2Interdisciplinary Program for Biomedical Sciences, Institute of Academic Initiatives, Suita, Japan

• Microarray analysis of lymph node subcapsularandmedullarysinus-lining lymphaticendothelialcells

• The microarray analysis revealed that CCL19 ishighly expressed in medullary sinus of lymphnodescomparedtosubcapsularsinus

• Identification and visualisation of CCL19+ lym-phatic endothelial cells using CCL19-reportermice


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W127

Macroscopic individual dynamics of vascular endothelial cells in angiogenesis

Naoko Takubo1, Kazuaki Naemura1,RyoYoshida2, Hiroki Kurihara1

1The University Of Tokyo, , Japan, 2The Institute of Statistical Mathematics, , Japan

• Weinvestigatedmacroscopicendothelialcell(EC)movements in angiogenesis show complex ECmovement includingtip cell rearrangement andcellmixing.

• IndividualECdynamicswerequantitativelyeval-uatedbysinglecellimagingformouseaorticringassay.

• U-turn movement, in which EC moves forwardandthenturnbackstothenewvesselbase,wasfound.

W128

Caspase-1 mediates pyroptosis through NLRP3-inflammasome activation in diabetic platelets

Meiling Su1, Xuejiao Fan1, Zhi Zeng1, Waiho Tang1

1Guangzhou Women And Children’s Medical Centre, Guangzhou, China

• The role ofmitochondrial ROS inNLRP3-inflam-masome activation has not yet been studied indiabeticplatelets.

• We investigated the inflammasome-dependentIL-1βreleaseindiabeticplatelet,anditscontribu-tiontoplateletpyroptosisandvascularcomplica-tionsindiabetes.

• NLRP3-inflammasome activation and IL-1β release was an indicator of platelet pyroptosis,whichcontributestovascularpermeabilityindia-betes.

W129

Activated platelets promote resolution of arte-rial injury repair through horizontal transfer of miR-143/145 and miR-223

Zhi Zeng1,LuoxingXia1, Xuejiao Fan1, Waiho Tang1

1Guangzhou Women And Children’s Medical Centre, Guangzhou, China

• ActivatedplateletsareinternalizedbyVSMCsandinhibit VSMC dedifferentiation by transferringplatelet-derivedmiR-143/145andmiR-223.

• WithreducedmiR-143/145andmiR-223 inDM,co-culturing activated DM plateletswith VSMCsdidnotsuppressVSMCdedifferentiation.

• Arterial wire injury exhibited reduced miR-143/145 and miR-223 levels, enhanced VSMCdedifferentiationandincreasedintimalhyperpla-sia.

W131

Delineating the role of cerebrovascular oxida-tive stress in Alzheimer’s disease

Anuradha Tarafdar1,AishaAlsheikhAbubaker2, Dina Vara1, GiordanoPula1

1University Of Exeter, Exeter, United Kingdom, 2University of Bath, Bath, United Kingdom

• Amyloidbeta(Aβ)peptideexposuretoendothe-lial cells leads to NADPH-oxidases (NOX) activa-tion and reactive oxygen species (ROS) genera-tion

• Aβpeptidecauseslooseningofintercellularjunc-tions in endothelial monolayers, compromisingthepermeabilityofbloodbrainbarrier(BBB)

• Thedamage toendothelial cellsby theAβ-pep-tide is inhibited by the NOX inhibitor diphenyl-eneiodonium(DPI)

W132

Single-cell RNA-seq and intravital microscopy of tumor-associated HEVs: specialized ves-sels for lymphocyte entry into tumors

Claire Tardiveau1,JulietteCoudert1,KrystleVeerman,Jean-PhilippeGirard1

1IPBS - CNRS, Toulouse, France

• Tumor-associatedHEVsaremolecularlyandmor-phologicallydistinctfromlymph-nodeHEVs

• Tumor-associatedHEVspresentsimilarfunctionstolymphnodeHEVs

• The tumormicroenvironment can directly influ-encethetumor-associatedHEVphenotype


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W133

Bi-specific extracellular matrix-directed pep-tide for tumor targeting

PrakashLingasamy1,PilleSäälik1,PäärnPaiste3, Toomas Asser4, Tambet Teesalu1,2

1University of Tartu, Tartu, Estonia, 2Cancer Research Center, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, USA, 3Department of Geology, University of Tartu, Tartu, Estonia, 4Department of Neurosurgery, Tartu University Hospital, Tartu, Estonia

• WeusedT7phagebiopanningtoidentifyabispe-cifictargetingpeptide,PL1,thattargetsfibronec-tin extra domain B (EDB) and tenascin-C FnIII Cdomain (TNC-C).

• Systemic PL1 functionalizednanoparticles hometo a panel of solid tumors in mice.

• PL1targetednanoparticlescanbeusedforimag-ingandtherapyofsolidtumorsinmice.

W134

Deciphering the mechanism of action of ApoB lipoproteins on endothelial cells

Hanoch Tempelhof1,KarinaYaniv1

1Weizmann Institute of Science, Rehovot, Israel

• Our newly established zebrafish apoB mutantsdisplay common hallmarks of human familialhypobetalipoproteinemia and abetalipoprotein-emia.

• apoB deficiency induces excessive angiogenesisphenotypesindifferentvascularbeds.

• ThehumanAPOB34truncatedformrescuesthevascular phenotypes, suggesting that this frag-ment contains the anti-angiogenic activity ofApoB.

W135

MPDZ promotes DLL4-induced Notch signal-ing during angiogenesis

Fabian Tetzlaff1,2, Andreas Fischer1,2

1German Cancer Research Center, Heidelberg, Germany, 2European Center for Angioscience, Mannheim, Germany

• MPDZ facilitates Notch signaling by promotingcell surface presentation of DLL1 and DLL4 andrecruitment to the adherens junction proteinNectin-2.

• MPDZ inhibits sproutingangiogenesis invitroaswellasinvivo.

• Loss of endothelial MPDZ expression induceschaotichypersproutinginsyngeneictumorscaus-inghypoxia.

W136

Mapping blood and lymphatic endothelial cell heterogeneity in the adult zebrafish

Yaara Tevet1, Roi Avraham1,KarinaYaniv1

1Weizmann Institute , Rehovot, Israel

W137

Autophagy protein 5 commands VEGFR2/eNOS phosphorylation and flow dependent control of endothelial functions

Olivia Lenoir1,2, Xavier Guillonneau3,4, Thomas Mathivet1,2,PierreNivoit1,2, Fadoua Montassar3,4, Avin Babataheri5,JunxiWu6,VéroniqueBaudrie1,2, Jennifer Bourreau7,8, Anne-Laure Guihot7,8, Emilie Vessieres7,8, Mathilde Lemitre1,2, Neeraj Dhaun1,6, Eric Camerer1,2, Anne Eichmann1,2,PatrickWFHadoke6,Jean-SébastienSilvestre1,2,AbdulI.Barakat6,PhilippeBonnin9, Daniel Henrion7,8, Pierre-Louis Tharaux1,2

1Inserm, Paris Cardiovascular Center - PARCC, Paris, France, 2Université Paris Descartes, Sorbonne Paris Cité, Paris, France, 3CNRS, Institut de la Vision, Paris, France, 4Université Pierre et Marie Curie, Sorbonne Universités, Institut de la Vision, Paris, France, 5Department of Mechanics, Hydrodynamics Laboratory (LadHyX), École Polytechnique, Palaiseau, France, 6BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, France, 7CNRS UMR 6214, Angers, France, 8INSERM U1083, Angers, France, 9Physiology – Lariboisière hospital, Assistance Publique-Hôpitaux de Paris, Paris, France

• Wedemonstratethatdefectiveendothelialauto-phagy,causedbydeletionofAtg5resultsinselec-tivelossofflow-inducedvasodilation.

• Pathological consequences: impaired flow-in-ducedremodellingandcardiacfunctionrecoveryafterinfarction.

• VEGFR2-dependent angiogenesis and signaling requireintactendothelialautophagy.


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W138

Flightless I regulation of pericyte function in diabetic wounds

Hannah Thomas1,2, Benjamin Hofma1,2,XantheStrudwick1, Stuart Mills1,2,AllisonCowin1,2

1University Of South Australia, Adelaide, Australia, 2CRC for Cell Therapy Manufacturing, Adelaide, Australia

• Flightless I (Flii) is a negative regulator of acutewoundhealing,withthepotentialtoalsoimpactdiabetichealing.

• Decreased Flii results in accelerated healing in a murine model of diabetes and increased pres-enceofpericytesinthediabeticwoundbed.

• Increased pericyte numbers coincide withenhanced angiogenesis and dampened inflam-mation,bothpositiveoutcomesforthehealingofdiabeticwounds.

W139

Therapeutic regulation of VE-Cadherin with a novel oligonucleotide drug for diabetic eye complications

Ka Ka Ting1,2,YangZhao1,2,WeiyongShen2,3,PaulColeman1,2,MissMichelleYam2,3, Tai-Loi Chan-Ling2, Jia Li1,2, Thorleif Moller4, Mark Gillies2,3,MathewVadas1,2, JenniferGamble1,2

1Centenary Institute, Camperdown, Sydney, Australia, 2The University of Sydney, Sydney, Australia, 3Save Sight Institute, Sydney, Australia, 4MirrX Therapeutics A/S, Coppenhagen, Denmark

• A novel drug, CD5-2, which increases endoge-nousVE-cadherinexpression, localises to vascu-larendothelialcellsintheeye

• CD5-2 reduces vascular leak, improves pericytecoverage,andmaintainsVE-cadherin integrity intheretinalvasculatureinthediabeticandprolif-erativemodelsofDR.

• CD5-2 inhibits microglia activation in diabeticmice.

W140

Deletion of VEGF-D leads to hyperlipidemia and delayed clearance of chylomicron rem-nants

Annakaisa Tirronen1, Taina Vuorio1,SannaKettunen1, Krista Hokkanen1,BastianRamms2, Henri Niskanen1, Hanne Laakso1,PyryI.Toivanen1, Minna U. Kaikkonen1,MattiJauhiainen3,PhilipL.S.MGordts2,SeppoYlä-Herttuala1,4

1A.I. Virtanen Institute, University of Eastern Finland, Kuopio, Finland, 2Department of Medicine, Division of Endocrinology and Metabolism, UCSD, San Diego, USA, 3National Institute for Health and Welfare, Genomics and Biomarkers Unit, Biomedicum, Helsinki, Finland, 4Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Deletion of VEGF-D in hyperlipidemic LDLR-/-ApoB100/100miceledtoincreasedplasmacho-lesterol and triglyceride levels but reduced ath-erogenesis

• Lipoprotein profile analysis and hepatic uptakestudies confirmed a delayed clearance of 100-500nmsizedchylomicronparticles

• Absence of VEGF-D signaling via VEGFR3 wasfoundtonegativelyregulatehepaticchylomicronremnantuptakeinaSyndecan1dependentman-ner

W141

Regulation of vascular remodeling by intricate interplay between blood flow and Notch

BartWeijts1,EdgarGutierrez1, Semion Saikin2, Ararat Ablooglu1, David Traver1,AlexGroisman1, Eugene Tkachenko1

1UCSD, San Diego, United States, 2Harvard University, Cambridge, United States

• Venous blood flow promotes the displacementofarterialendothelialcellsbyvenousendothelialcellsduringthetransformationofintersegmentalarteries into veins.

• Arterialbloodflowpreventing thedisplacementof arterial endothelial cells in intersegmental ves-selswhichremainarteries.

• Arterial blood flow also protects intersegmentalarteries from anastomosis with venous sproutsthrough Notch activation in arterial endothelialcells.


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W142

The phenotype of cardiac tissue-resident macrophages is determined by heme oxygen-ase-1

Mateusz Tomczyk1,IzabelaKraszewska1, Neli Kachamakova-Trojanowska1,WitoldNowak1, Alicja Jozkowicz1, Jozef Dulak1,2,AgnieszkaJazwa-Kusior1

1Department of Medical Biotechnology, Faculty of Biochemistry, Biophysics and Biotechnology, Jagiellonian University, Krakow, Poland, 2Kardio-Med Silesia, Zabrze, Poland

• The absence of heme oxygenase-1 (HO-1)increases turnover of cardiac macrophages (cMΦs)andaltersthebloodcytokineprofilefol-lowingmyocardialinfarction(MI).

• Better post-MI survival of HO-1-/-mice in com-parisontotheirwild-typelittermatesisabolishedwhenmacrophagedepletionprecedesMI.

• HO-1-deprived neonatal cMΦ are unable torespond to CO stimulation and exhibit a proin-flammatory-likephenotype.

W143

Role of CAD-associated genetic variation in the regulation of cell type specific enhancer activity

Anu Toropainen1,IlakyaSelvarajan1,CaseyRomanoski2, Markku Laakso3,MinnaKaikkonen-Määttä1

1A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, 2University of Arizona, Tucson, USA, 3University of Eastern Finland, Kuopio, Finland

• Mostofthecoronaryarterydisease–associatedsingle nucleotide polymorphisms (SNPs) arelocated at non-coding regions of the genome.

• SNPslocatedatenhancerspotentiallyaltertran-scriptionfactorbindingandthusmodulatetran-scriptionaloutput.

• Weaimto interpretthefunctionalroleoftheseenhancer variants in coronary artery disease byidentifying genes they regulate and pathwaysbeingaffected.

W144

Cross talk between endothelial cell and pros-tate cancer cell through paracrine factors

Verónica Torres-Estay1, s Catalina Asencio1,PaulaSotomayor1, Julio Amigo1,Alejandro.SGodoy1,3

1Pontificia Universidad Católica de Chile, Santiago, Chile, 2Universidad Andrés Bello, Santiago, Chile, 3Roswell Park Comprehensive Cancer Center , Buffalo, United States

• Paracrine factor from endothelial cells promoteproliferation,migration and invasion of prostatecancer cell lines.

• Endothelial cells, either through cell-to-cell inter-action or through paracrine communication,enhancedprostatetumorgrowth.

• Endotheliumcouldcontribute to theacquisitionof a more advanced and/or metastatic pheno-typeofprostatecancer.

W145

Optimization of differentiation of adipose tis-sue-derived stem cells into vascular smooth muscle cells

Martina Trávníčková1,2,JanaMusílková1,MartinMolitor3, LucieBačáková1

1Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic, 2Second Faculty of Medicine, Charles University, Prague, Czech Republic, 3Department of Plastic Surgery, Bulovka Hospital, Prague, Czech Republic

• Optimizingthemediumcompositionfordifferen-tiationofASCstowardsVSMCs(TGFβ1andBMP4addition)wasstudiedinstaticcultureconditions.

• Theproliferationofthecellsandimmunofluores-cence staining of smooth muscle markers (α-ac-tin,calponin,desmin)wereevaluated.

• TGFβ1 and BMP4 supported the proliferation.The number of α-actin- and calponin-positivecellsincreasedintimeperiodoftheculture.


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W146

Preliminary studies for application of PLGA particles as drug carriers to endothelial cells

Reginaldo Almeida Trindade1,2, Henk Moorlag1, Manon Woest1, G Molema1, Jan Kamps1

1The Endothelial Biomedicine & Vascular Drug Targeting research group (EBVDT), Department of Pathology and Medical Biology, Medical Biology section, University Medical Center Groningen (UMCG), University of Groningen, Groningen,, Netherlands, 2Laboratory of ImmunoParasitology (LIPA), Department of Toxicological and Clinical Analysis (DACT), Faculty of Pharmacy, Federal University of Rio de Janeiro (UFRJ), Rio de Janeiro,, Brazil

• PLGAparticlesasdrugcarrierstoendothelialcellstotreatsystemicinflammation;

• CytotoxicanalysisofPLGAparticlesonendothe-lialcells;

• Interaction index between PLGA particles andendothelial cells.

W147

Identification of shear stress-responsive enhancers in endothelial cells

Roman Tsaryk1, Noelia Diaz1, Olga Bondareva2, Elvin V. Leonard1,HansSchnittler2,JuanMVaquerizas1, Arndt F Siekmann1

1Max Planck Institute For Molecular Biomedicine, Münster, Germany, 2Institute of Anatomy and Vascular Biology, Wilhelms-University of Münster, Münster, Germany

• Shearstress regulates theactivationanddeacti-vationofgeneenhancers

• Activated gained enhancers spatially associatedwith genes upregulated by flow, while deacti-vated lostenhancersassociatedwithdownregu-lated genes

• Enhancer flow responsiveness was confirmedthroughinvitroluciferasereporterassays

W148

Direct reprogramming of human fibroblasts into vascular progenitors via manipulation of the cell metabolism

Marianna Tsifaki1, Rachel Caines1, Marta Vila Gonzalez1, Diana Drehmer1,AmyCochrane1, Sophia Kelaini1, David Grieve1,AndrianaMargariti1

1The Wellcome-Wolfson Institute For Experimental Medicine, Queen’s University Of Belfast, Belfast, United Kingdom

• Directly reprogramming human fibroblasts intovascularprogenitorsasastrategyofregeneratingthe vasculature,

• Themanipulationofthecellmetabolismiscrucialtothesuccessfulre-writingofcellfate,

• Lessons learned from in vivo regeneration willpavethewayfortheproductionofmultiplesta-blecelllines

W149

Specific targeting of PDGFRβ inhibits growth and angiogenesis of tumors with high PDGF-BB expression

Maria Tsioumpekou1,2, Sara Cunha3, Haisha Ma4, Aive Åhgren1, Carl-Henrik Heldin1, Johan Lennartsson2

1Department of Medical Biochemistry and Microbiology, Uppsala University, , Sweden, 2Department of Pharmaceutical Biosciences, Uppsala University, , Sweden, 3Department of Immunology, Genetics and Pathology, Uppsala University, , Sweden, 4Department of Neuroscience, Uppsala University, , Sweden

• Specific targeting of PDGFRβ inhibits growth ofhighPDGF-BBexpressingtumorsmoreefficientlythantheclinicallyusedPDGFinhibitorimatinib

• SpecifictargetingofPDGFRβ results in decreased vesseldensity,-size,-functionandpericytecover-ageinhighPDGF-BBtumor-bearingmice

• Levels of tumor PDGF-BB may serve as a bio-marker for selectionof cancerpatients for anti-PDGFtherapy


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W150

Establishment of an in vivo model to observe patient-derived tumor blood vessels.

Yohei Tsukada1, Fumitaka Muramatsu1, Hisamichi Naito1, HiroyasuKidoya1,NobuyukiTakakura1

1Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, 3-1 Yamada-oka, Suita, Japan

• Usingapatient-derivedtumor,weestablishedaninvivomodelwithhumantumorbloodvessels.

• We can observe human tumor blood vessels atmultipletimepoints.

• This model is a useful tool for evaluating theeffectofdrugstargetinghumantumorbloodves-sels in vivo.

W151

Modulation of endothelial glucose transport and metabolism by quercetin and HIF-1-alpha signalling

Sarka Tumova1, Asimina Kerimi1,GaryWilliamson1

1University Of Leeds, Leeds, United Kingdom

• Circulating polyphenol metabolites can affectendothelialphysiologyandconsequentlycardio-vascular health.

• Polyphenol quercetin affected glucose uptakeandgeneexpressioninamannerdistinctfromitsconjugates.

• QuercetinincreasedHIF-1-alphastabilityindicat-ing a potential to regulate endothelial glucosemetabolism.

W152

Perivascular adipose tissue controls insu-lin-stimulated perfusion and glucose uptake in muscle through adipomuscular microvascular anastomoses

Alexander H Turaihi1, Erik H Serné1,CarlaFMMolthoff,JasperJKoning,HansWNiessen,MarieJoseTHGoumans,ConnieJJimenez,JohnSYudkin,YvoMSmulders,VictorWMvanHinsbergh,EttoCEringa1Vumc, , Netherlands

• PVATwithinmuscle regulatesmuscle perfusion,glucoseuptakeandmuscleproteinexpression.

• PVATcommunicateswiththedistalmicrocircula-tionviamicrovascularadipomuscularanastomo-ses.

W153

Role of brain pericytes in the regulation of leukocyte trafficking under homeostatic and pathological conditions

Orsolya Török1,BettinaSchreiner2, Annika Keller1

1Department of Neurosurgery, University Hospital Zürich, Zürich, Switzerland, 2Institute of Experimental Immunology, University of Zürich, Zürich, Switzerland

• Naïve pericyte-deficient mice show increasednumber of infiltrating immune cells in the CNSparenchyma.

• Inductionofexperimentalautoimmuneencepha-lomyelitis(EAE)inpericyte-deficientmiceresultsinanatypicalEAEphenotype.

• EAEinpericyte-deficientmiceisaccompaniedbyan increasedmonocyte infiltration compared tocontrols.

W154

Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia

Kari Vaahtomeri1,2,MarkusBrown1,RobertHauschild1, Ingrid De Vries1,AlexanderLeithner1,MatthiasMehling1, WalterKaufmann1,MichaelSixt1

1Institute of Science and Technology Austria (IST Austria), Klosterneuburg, Austria, 2Translational cancer biology program, research programs unit, University of Helsinki and Wihuri Research Institute, Helsinki, Austria

• Dendritic cell entry into lymphatic capillaryinduceschemokineCCL21secretiontoendothe-lialjunctions.

• Directcontactbydendriticcells inducescalciumsignallinginlymphaticendothelialcells.

• Dynamic rather than pre-patterned chemokineCCL21cuespromoteDCtransmigration.

W155

Pump it up – an innovative approach for long-term cell cultivation under flow

Helga Wagner1,WolfgangÖffner1, Irina Hein1, Roman Zantl1

1ibidi GmbH, Martinsried, Germany

• cellcultivationunderflow• long-term shear stress• endothelial cells


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W156

Induction and Establishment of Kidney Vascu-lature System

Seppo Vainio1, Kimmo Halt1, Susanna Kaisto1, Zenglai Tan1, IlyaSkovorodkin1

1Biocenter Oulu & Infotech Oulu, Oulu, Finland

• Kidney has CD146+ progenitor cells responsibleofthekidneyvasculature

• Kidneyglomeruluscanbeassembledbyinducionofflow

• Kidneyvasculaturecanbefatemappedandfucn-tionallystudiedbyusingkidneyprimordiadisso-ciationandorganreconstitution

W157

Inducible ablation of retinal pigment epithe-lium results in progressive loss of choroidal vasculature in mice

Taku Wakabayashi1, Hisamichi Naito2,NobuyukiTakakura2, Kohji Nishida1

1Department of Ophthalmology, Osaka University Graduate School Of Medicine, Suita, Japan, 2Department of Signal Transduction, Research Institute for Microbial Diseases, Osaka University, Suita, Japan

• Generation of mouse model of retinal pigmentepithelial loss

• Lossofretinalpigmentepitheliumresultsincho-roidalatrophy

• Themouse represents themodelofdryage-re-latedmaculardegeneration

W158

EGFL7 mediates BMP9-induced sprouting angiogenesis of endothelial cells derived from human embryonic stem cells

Gudrun Valdimarsdottir1, Anne Richter1, MSc. Svala Magnus1,TobiasRichter1,MasatoMorikawa2,AnZwijsen3

1University of Iceland, Reykjavik, Iceland, 2Ludwig Institute for Cancer Research, Uppsala, Sweden, 3KU Leuven Department of Cardiovascular Sciences, Leuven, Belgium

• BMP9/ALK1 signalling induces sprouting ofhESC-derived endothelial cells.

• EGFL7mediatesBMP9-inducedsproutingangio-genesis.

• EGFL7inhibitstheNOTCHpathwayandactivatestheERKpathway

W159

Microparticles harboring sonic hedgehog enhance vasculogenesis capacity of endothe-lial progenitor cells from myocardial infarction patients

CarlosBueno-Betí1,2, Susana Novella1,2,RaffaellaSoleti3, Ana Mompeon1,2, Luisa Vergori3, Juan Sanchis2,4, Ramaroson Andriantsitohaina3,MaríaCarmenMartinez3, Carlos Hermenegildo1,2

1Dep. Physiology, Fac.Medicine & Dentistry. University of Valencia, Valencia, Spain, 2INCLIVA Biomedical Research Institute, Valencia, Spain, 3INSERM UMR1063, Stress oxydant et pathologies métaboliques, Université d’Angers, Angers, France, 4Cardiology Department, Hospital Clínico Universitario and Dep. Medicine, Fac. Medicine & Dentistry. University of Valencia, Valencia, Spain

• MPShh+increaselateEPCvasculogenesiscapac-itythroughShhpathway.

• InEPCisolatedfromperipheralbloodofpatientssuffering acute myocardial infarction (AMI) thevasculogenic ability is impaired, and restoredafterexposuretoMPShh+.

• We proposed EPC exposed to MPShh+ as apotentialtherapeutictoolforimprovingvascularregenerationafterischemicdiseasessuchasAMI.

W160

New consideration of lymphatic endothelial cells as key actors of the tissue microenviron-ment

Maureen Van De Velde1,MarieEbroin1, Silvia Blacher1, MelissaGarcía-Caballero1, Frederic Kridelka2, Agnès Noel1

1University of Liege, Giga-Cancer, LBTD, Liège, Belgium, 2Department of Obstetrics and Gynecology, CHU Liege, Liège, Belgium

• The direct confrontation of lymphatic endothe-lial cell (LEC)monolayers to different carcinomacell linesdisturbs theendothelium integrityandimpairscell-celljunctions.

• “ActivatedLEC”bytumorcellsmodifytheirtran-scriptomicprofileleadingtoIL-6secretionbyLEC.

• IL-6 LEC-derived promotes tumor cell prolifera-tionendowingLECwithakey role in the tumormicroenvironment.


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W161

Endothelial glucose metabolism regulates glycocalyx hyaluronan synthesis and thereby vessel stability

Bernard Van Den Berg1,GangqiWang1, Margien Boels1, Anna-Rita Cantelmo2,3,SarantosKostidis4,CristinaAvramut5, Erik Jansen6, Gesa Tiemeier1, Eelco de Koning1,6, WendySol1,WilliamAird7,FranckLebrin1, Johan van der Vlag8, Anton-Jan van Zonneveld1, Hermann-Josef Groene9, Hans Vink10,PeterCarmeliet2,3,TonRabelink1

1The Einthoven Laboratory for Vascular and Regenerative Medicine, Division of Nephrology, LUMC, Leiden, Netherlands, 2Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, Leuven, Belgium, 3Laboratory of Angiogenesis and Vascular Metabolism, Vesalius Research Center, Leuven, Belgium, 4Center for Proteomics & Metabolomics, LUMC, Leiden, Netherlands, 5Department of Molecular Cell Biology, Section Electron Microscopy, LUMC, Leiden, Netherlands, 6Hubrecht Institute / KNAW and UMC, Utrecht, Netherlands, 7Center for Vascular Biology Research, Division of Molecular and Vascular Medicine, BIDMC, Boston, United States of America, 8Nijmegen Centre for Molecular Life Sciences, Department of Nephrology, RUMCN, Nijmegen, Netherlands, 9Department of Cellular and Mol;ecular Pathology, The German Cancer Research Center, Heidelberg, Germany, 10Department of Physiology, MUMC, Maastricht, Netherlands

• Endotheliallossofhas2leadstoglomerulopathy,retinopathy and cardiomyopathy due to vesseldestabilization.

• Increasing intracellular concentrations of UDP-GlcAandUDP-GlcNAcresultinincreasedHApro-ductioninahas2dependentmannerinvitro.

• Silencing the glycolytic activator PFKFB3, with-out changing total HAS2 protein levels, in turn increases luminalendothelialHAcoverage,bothin vitro and in vivo.

W162

Combined laser microdissection and trans-lating ribosome affinity purification provides high-resolution glomerular-specific endothe-lial cell transcriptomes

Martijn van der Ent1,PeterZwiers2,ElianePopa2, David Ginsburg1,3, Grietje Molema2,AudreyCleuren1

1University Of Michigan, Ann Arbor, United States, 2University Medical Center Groningen, Groningen, the Netherlands, 3Howard Hughes Medical Institute, Ann Arbor, United States

• Laser microdissection combined with endothe-lial cell translating ribosome affinity purificationyields enhanced resolution microvascular tran-scriptomes.

• Characterization of in vivo endothelial cell het-erogeneityalongthevasculartree.

• Identification of glomerular endothelial-specificmarker.

W163

Long-term Vitamin K antagonist treatment induces calcification and atherosclerotic plaque progression, promoting a prethrom-botic state.

Rick H. Van Gorp1,2, Armand M.G. Jaminon1, Constance C. Baaten1,JohanW.Heemskerk1,ChrisP.Reutelingsperger1, Henri M.H. Spronk1, Leon J. Schurgers1

1Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre,, Maastricht, Netherlands, 2Nattopharma ASA, Høvik, Norway

• Long-termVKA treatment inducesmacrocalcifi-cationandcorrelateswithatherogenesisandpro-longedprothrombintime.

• VascularcalcificationstimulatesaprethromboticstatebyincreasingfactorIXa:antithrombinlevels.

• CalcifiedVSMCunderflowincreasesfibrinforma-tionwhichispreventedbyinhibitorsoftheintrin-sicorextrinsiccoagulationpathway.

W164

Pleiotrophin as a target for vascular normal-ization therapy in glioblastoma

Luuk Van Hooren1,AnnaDimberg1

1Department of Immunology, Genetics and Pathology; Uppsala University, Uppsala, Sweden

• Pleiotrophin is adriverof vascular abnormaliza-tioninglioma

• Protein constructs of Pleiotrophin merged withthioredoxin can be used to induce endogenousanti-Pleiotrophinantibodies

• RNA sequencing of endothelial cells isolatedfromPleiotrophinexpressinggliomasiscurrentlyunderway in order to characterize the vascularabnormalizationonageneexpressionlevel


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W165

Myeloid PHD2 knockdown drives macrophage apoptosis and collagen secretion of fibro-blasts/smooth muscle cells in atherosclerosis

Kim Van Kuijk1, Thomas Theelen1, Elke Marsch1, Jasper Demandt1,MarionGijbels1, Han Jin1, Chris Reutelingsperger1, Judith Cosemans1, Leon Schurgers1, PeterCarmeliet2, Erik Biessen1, Mat Daemen3, Judith Sluimer1

1Maastricht University, Maastricht, Netherlands, 2VIB&KU, Leuven, Belgium, 3AMC Amsterdam, Amsterdam, Netherlands

• PHD2 knockdown mice show decreasedintraplaquemacrophagecontent,possiblycausedbyhypoxia-dependentincreaseinapoptosis.

• Myeloid PHD2 knockdown leads to an increaseinfibrosis,possiblycausedbyparacrinesignalingbetween macrophages and fibroblasts/smoothmuscle cells.

• Human PHD2 protein is correlated withmacro-phagemarkerCD68and increaseswithworsen-ing of disease.

W166

Putative Brain Lymphatic Endothelial Cells in Mice

Max van Lessen1,2,3, Manuela Cerina4,5, Stefan Schulte-Merker1,2,3

1Institute of Cardiovascular Organogenesis and Regeneration, WWU Münster, Münster, Germany, 2Faculty of Medicine, WWU Münster, Münster, Germany, 3Cells-in-Motion Cluster of Excellence, WWU Münster, , Germany, 4Department of Neurology, WWU Münster, Münster, Germany, 5Institute of Translational Neurology, WWU Münster, Münster, Germany

• Brainlymphaticendothelialcells• Cellswithlymphaticandmacrophageidentity• Wasteclearancefromthebrain

W167

Quantifying extracellular matrix deformations and cellular forces around angiogenic sprouts

Marie-MoVaeyens1,AlvaroJorge-Peñas1,TommyHeck1,ChristianSteuwe2,MaartenRoeffaers2, Hans Van Oosterwyck1,3

1Biomechanics Section, Department of Mechanical Engineering, KU Leuven, Leuven, Belgium, 2Center for Surface Chemistry and Catalysis, KU Leuven, Leuven, Belgium, Leuven, Belgium, 3Prometheus, division of Skeletal Tissue Engineering, KU Leuven, Leuven, Belgium, Leuven, Belgium

• We have established methods to quantify 3Dcell-induced extracellular matrix deformationsand cellular forces around angiogenic sprouts in collagen

• Wefoundthatcellularforcesarelocalizedatthesprouttips(between10-50nN)andbase(around300 nN)

• Our analyses can help in detecting mechano-transduction sites, which may co-localise withhighmatrixdeformationorcellularforces

W168

Border control at the vessel wall: Preferred exit-sides for leukocyte diapedesis.

Bram Van Steen1, Ivar Noordstra1, Lilian Schimmel1, Jaap van Buul1

1Molecular Cell Biology Lab, Dept. Plasma Proteins, Sanquin Research and Landsteiner Laboratory, Academic Medical Center, Amsterdam, the Netherlands. , Amsterdam, Netherlands

• Leukocytetransmigrationthroughthebloodves-selwallisnotrandomlydistributed.

• Neutrophils show a preference for specific exitsites when migrating through a monolayer inbloodvesselmodelunderflow.

• Data indicate that local leukocyte-endothelialeventsarerequiredtoprimeendothelialcellstorecognizealocalexitsitefordiapedesis.


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W169

Loss of endothelial glycocalyx hyaluronan induces excessive angiogenesis after femoral artery ligation

Gangqi Wang1, Margreet de Vries2,WendySol1, Annemarie van Oeveren-Rietdijk1,HettydeBoer1, Anton-Jan van Zonneveld1,PaulQuax2,TonRabelink1, Bernard van den Berg1

1The Einthoven Laboratory for Vascular and Regenerative Medicine, Division of Nephrology, LUMC, Leiden, Netherlands, 2Department of Surgery, LUMC, Leiden, Netherlands

• Has2-cKO mouse calf muscle capillary densityincreasedsignificantlymoreuponfemoralarteryligationcomparedtocontrol.

• KnockdownofHAS2inendothelialcellsresultsinincreased angiogenesis in vitro.

• Quiescent endothelial cells express a thick HAsurface coat.

W170

Role of endothelial Piezo1 in flow sensing and barrier regulation

Shengpeng Wang1,NinaWettschureck1, Stefan Offermanns1


• EndothelialP2Y2andGq/G11isessentialforflowdependent endothelial responses in vitro and regulationofvasculartoneandbloodpressureinvivo.

• Themechanosensitive cation channel Piezo1 asupstream mechanism for fluid shear stress-in-ducedATP release and subsequentP2Y2activa-tion

W171

A molecular atlas of cell types and zonation in the brain vasculature

Michael Vanlandewijck1,2,LiqunHe2,3, Maarja Andaloussi Mäe2, Johanna Andrae2,Msc.KhayrunNahar2, Koji Ando2, Christer Betsholtz1,2

1Integrated Cardio Metabolic Centre, Karolinska Institute, Huddinge, Sweden, 2Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 3Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin, China

• Weprovidemoleculardefinitions for theprinci-paltypesofbloodvascularandvessel-associatedfibroblast-likecellsintheadultmousebrain.

• The transcriptional basis of the gradual phe-notypic change along the arteriovenous axis isestablished

• Pericytesareorganotypic

W172

hiPSCs in vitro endothelial differentiation via a bi-potent hemangiogenic progenitor, the hemangioblast.

Alejandra Vargas-Valderrama1,2,DenisClay1, Guillaume Ha1,4, Georges Uzan1, Maria Teresa Mitjavila Garcia1, Hind Guenou1,3

1UMRS-MD 1197, Villejuif, France, 2Université Paris Sud. Université Paris-Saclay, Orsay, France, 3Université d’Evry-Val-d’Essonne. Université Paris-Saclay, Evry, France, 4Université Paris Diderot. , Paris, France

• Duringembryogenesis,endothelialandhemato-poieticcellsdevelopthroughacommonancestor,thehemangioblast.

• ACD309+CD144+populationwas isolatedfrom3,5-dayhiPSCs-derivedembryoidbodiesandcul-turedeitherunderendothelialorhematopoieticconditions.

• Functional endothelial and hematopoietic cellswere obtained from this isolable bipotent cellsthatcouldbeusedtomedicineregenerative.


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W173

Pericyte insulin signalling modulates sprout-ing angiogenesis, venous development, and angiopoietin expression.

Nele Warmke1,AndrewMNWalker1,ClaireHOzber1, KathrynJGriffin1,NadiraYYuldasheva1, Richard M Cubbon1

1Leeds Institute of Cardiovascular and Metabolic Medicine, University of Leeds, Leeds, United Kingdom

• Lossofpericyteinsulinsignallingincreasesendo-thelial tip cell formation, peri-venous vascular-ity, and venous diameter during developmentalangiogenesis.

• Thisphenotype isnotassociatedwithabnormalexpressionof classical arterial and venous com-mitment markers.

• Abnormal expression of angiopoietin-1 and -2suggestsabnormalpericyte-endothelial commu-nicationmayunderpinthephenotype.

W174

Establish an early detection tool to enable monitoring LECs turnover during normal physiology and pathologies

Gili Wellner1

1Weizmann Institute, Rehovot, Israel

• We use tissue-specific methylation patterns incell-free circulating DNA (cfDNA) to detect LECdeathindifferentpathologicalconditions.

• We FACS isolated lymphatic endothelial cells(LECs)fromfreshhumantissueusingdoubleanti-body staining and submitted them to Illuminasequencing

• Deciphering LEC dynamics may serve as a sen-sitive early detection tool for lymphatic-related pathologies.

W175

CD93-MMRN2 interaction regulates endothe-lial cell dynamics and fibronectin fibrillogene-sis by enhancing integrin-β1 activation

Kalyani Vemuri1,RobertaLugano1,DiYu1, Magnus Essand1,StaffanJohansson2,ElisabettaDejana1,3, Anna Dimberg1

1Department of Immunology, Genetics and Pathology, Science for Life Laboratory, Uppsala University, The Rudbeck Laboratory, Uppsala, Sweden, 2Department of Medical Biochemistry and Microbiology, Uppsala University, Uppsala, Sweden, 3Vascular Biology Unit, FIRC Institute of Molecular Oncology, Milan, , Italy

• MMRN2protectsCD93fromproteolyticcleavageandstabilizesCD93attheplasmamembrane

• Interaction with MMRN2 localizes CD93 to theendothelialmigratingfrontandanchorsCD93totheextracellularmatrix

• The CD93-MMRN2 complex is required for effi-cient integrin-β1activationandfibronectinfibril-logenesis

W176

Investigating Vascular Niches of Glioblastoma by Spatial Transcriptomics

Marie Duhamel1,JunbinQian1, Linqian Weng1, Diether Lambrechts1,GabrieleBergers1,2

1VIB-Center for Cancer Biology, Department of Oncology, Katholieke Universiteit Leuven, Leuven, Belgium, 2Department of Neurological Surgery, Brain Tumor Research Center, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, USA

• Glioblastoma are genetically and phenotypicallyheterogeneous tumors.

• Glioblastomas contain distinct vascular nicheswithdifferentcompositionsandfunctions.

• Spatial transcriptomics of intratumor-hetero-geneous GBMs reveal the interaction of tumorcloneswiththedistinctniches.


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W177

Role of VEGFR2 activation in regulating lym-phatic density and function.

Lakshmi Venkatraman1, Miguel Sainz-Jaspeado1, Steven Proulx2, Michael Detmar2,LenaClaesson-Welsh1

1Department Of Immunology, Genetics And Pathology, Uppsala University , Uppsala, Sweden, 2Department of Chemistry and applied Biosciences ,ETH , Zürich, Switzerland

• VEGFR2 mutant (Y949F) mice have higher lym-phaticvesselandvalvedensitycomparetocon-trols.

• Y949F models injected with B16F10 melanomashowdecreasedlymphnodemetastasis.

• 3. VE-cadherindistributioninbuttonandzipperjunctionsisanalysedinY949FandWTmice.

W178

Role of coronin1B on the regulation of the endothelial function and angiogenesis

Ann-Cathrin Werner1, Melanie Salvermoser1,BettinaPitter1, Jiahui Cao2,Hans-JoachimSchnittler2,BettinaSchmid3,BarbaraWalzog1, Eloi Montanez1

1Walter Brendel Center of Experimental Medicine, Institute of Cardiovascular Physiology and Pathophysiology, Biomedical Center, LMU Munich, 82152 Planegg-Martinsried, Germany, 2Institute of Anatomy and Vascular Biology, Westfälische Wilhelms-Universität Münster, 48149 Münster, Germany, 3German Center for Neurodegenerative Diseases (DZNE), 81377 Munich, Germany

• Coronin1B is enriched at lamellipodia, cell-cell junctions and junction associated intermittedlamellipodia (JAIL)

• Coronin1B is localized to cell-cell junction in anactindependentmanner

• Coronin1Bisrequiredforinvitroangiogenesis

W179

FOXOs coordinate cell cycle behavior and specification of lymphatic endothelial cells

Kerstin Wilhelm1,InesMartinez-Corral2,ChenyueShi1, RonaldA.DePinho3, Taija Mäkinen2,MichaelPotente1

1Max Planck Institute For Heart And Lung Research, Bad Nauheim, Germany, 2Department of Immunology, Genetics and Pathology, Uppsala University, Uppsala, Sweden, 3Dana-Farber Cancer Institute, Boston, USA

• Loss of FOXOs in the lymphatic endotheliumcausesamassivelymphaticovergrowth.

• FOXO-deficient lymphatics are immature, lackvalves and are devoid of mural cell support.

• FOXOs are crucial transcriptional regulatorsof lymphatic development coupling cell cycledynamicsandspecificationprogramsinlymphat-ics.

W180

Macrophage-resident Neuropilin-1 promotes adipose tissue vascularization during weight gain and protects against metabolic syn-drome

Ariel Wilson1, Zhuo Shao1, Vanessa Grenier1, Gaëlle Mawambo1, Jean-François Daudelin1, Agnieszka Dejda1, FrédériquePilon1,CéliaParinot1,MalikaOubaha1, Nathalie Labrecque1, Vincent de Guire1,FlorianSennlaub2, Jean-SébastienJoyal3, Michel Meunier4,PrzemyslawSapieha1

1Maisonneuve-Rosemont Research Center, Montreal, Canada, 2Institut National de Santé et Recherche Médicale, Paris, France, 3Centre Hospitalier Universitaire Ste-Justine, Montreal, Canada, 4École Polytechnique, Montreal, Canada

• Neuropilin-1 (NRP1) expressing myeloid cellsdriveadiposetissuevascularization.

• NRP1+myeloidcellsregulateweightgaininobe-sity.

• TherapeutictransferofNRP-1+bonemarrowres-cuesaprediabeticphenotype.

W181

Activating mutations in PIK3CA are specifi-cally localized in lymphatic malformation-de-rived lymphatic endothelial cells: therapeutic implications

Jörg Wilting1

1Institute of Anatomy and Cell Biology, Göttingen, Germany

• PIK3KCAmutationsarespecificallylocatedinLECsoflymphangiomas.

• Newactivatingmutationswereidentified.• Kinaseinhibitorsshowbeneficialclinicaleffects.


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W182

GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis

CyrillGéraud1,2,Philipp-SebastianKoch1,2, Johanna Zierow1,2, Manuel Winkler1,2, Theresa Staniczek1,2, Sina WietjeKürschner1,2,KayKlapproth3, Karin Busch3, Victor Olsavszky1,2,ThomasLeibing1,2,AlexandraDemory1,2, FriederikeUlbrich1,2,MiriamDiett1,2,SandhyaSingh1,2, CarstenSticht4, Katja Breitkopf-Heinlein5, Karsten Richter6, Sanna-Maria Karppinen7,TainaPihlajaniemi7, Bernd Arnold8,Hans-ReimerRodewald3,HellmutG.Augustin2,9,10, KaiSchledzewski1,2, Sergij Goerdt1,2

1Department of Dermatology, Venereology and Allergology, University Medical Center and Medical Faculty Mannheim, University of Heidelberg, Center of Excellence in Dermatology, Mannheim, Germany, 2European Center for Angioscience, Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany, 3Division of Cellular Immunology, German Cancer Research Center (DKFZ), Heidelberg, Germany, 4Center for Medical Research, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, 5Department of Medicine II, Section Molecular Hepatology, Medical Faculty Mannheim, Heidelberg University, , Germany, 6Division of Molecular Genetics, DKFZ, , Germany, 7Faculty of Biochemistry and Molecular Medicine and Biocenter Oulu, University of Oulu, , Finland, 8Division of Molecular Immunology, DKFZ, , Germany, 9Division of Vascular Oncology and Metastasis (DKFZ-ZMBH Alliance), DKFZ, , Germany, 10Department of Vascular Biology and Tumor Angiogenesis (CBTM), Medical Faculty Mannheim, Heidelberg University, , Germany

• TheStab2-CredrivermouseisanECsubtype-spe-cificCremousethatallowsLSEC-specificgeneticmodificationsinvivo.

• LSEC-restricteddeletionofGata4 leads to capil-larizationofthelivermicrovascularendothelium.

• Gata4 acts as molecular master regulator of hepaticmicrovascularspecificationwhichisindis-pensableforliverdevelopment.

W183

Primary Cilia Sensitize Endothelial Cells to BMP and Prevent Excessive Vascular Regres-sion

Anne-clemence Vion1,2, Silvanus Alt1,AlexandraKlaus-Bergmann1,2,AnnaSzymborska1,2,TuyuZheng1, Tijana Perovic1, Adel Hamouten3,4, Marta Bastos Oliveira1, Eireen Bartels-Klein1,2,IreneHollfinger1,rPierre-EmmanuelRautou3,4,5,MiguelO.Bernabeu6,7, Holger Gerhardt1,2,8,9

1Max Delbrück Center For Molecular Medicine, Berlin, Germany, 2DZHK (German Center for Cardiovascular Research), , Berlin, Germany, 3INSERM, U970, Paris Cardiovascular Research Center - PARCC, Paris, France, 4Université Paris Descartes, Sorbonne Paris Cité, Paris, France, Paris, France, 5DHU Unity, Pôle des Maladies de l’Appareil Digestif, Service d’Hépatologie, Centre de Référence des Maladies Vasculaires du Foie, Hôpital Beaujon, , Paris, France, 6Centre for Medical Informatics, Usher Institute, The University of Edinburgh, Edinburgh, United Kingdom, 7Centre for Computational Science, Department of Chemistry, University College London, London, United Kingdom, 8Vascular Patterning Laboratory, VIB Center for Cancer Biology, Leuven, Belgium, 9Berlin Institute of Health (BIH), Berlin, Germany

• Endothelialprimaryciliaaremainlyfoundinlowshear stress areas of the vasculature

• TheprimaryciliumfacilitatesBMP9responsesinendothelialcellsunderlowshearstress

• Primary cilia maintain collective polarization ofendothelialcellsunderlowshearstress,prevent-ingexcessivevascularregression.

W184

Distinct microvascular responses associate with strain-dependent patterns of ischemic muscle damage and regeneration

Galina Wirth1,PetraKorpisalo1,SeppoYlä-Herttuala1

1University Of Eastern Finland, Kuopio, Finland

• We compared ischemic skeletalmuscle damagein relation to perfusion restoration and micro-vascularresponsesbetweenelderlyC57Bl/6JandLDLR-/-ApoB100/100mice,

• The endogenous skeletal muscle response to ischemic injurydiffersbetweenelderlyC57Bl/6JandhyperlipidemicLDLR-/-ApoB100/100mice,

• The degree of muscle injury and regenerationseemstobeinfluencedbytheprimarymicrovas-cularresponseratherthanthequantityofbloodflow.


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W185

Endothelial Notch signaling controls angio-kine-mediated metabolic zonation and metas-tasis in the liver

Sebastian Wohlfeil1, Verena Häfele1,KaiSchledzewski1, Mrs.JohannaZierow1,Mr.VictorOlsavszky1,Philipp-SebastianKoch1,CyrillGéraud1,2,3, Sergij Goerdt1,3

1Department of Dermatology, Venereology, and Allergology, University Medical Center and Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, 2Section of Clinical and Molecular Dermatology, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany, Mannheim, Germany, 3European Center for Angioscience, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany

• EnhancedNotchsignaling inhepaticendothelialcells (HEC) effaced regular liver endothelial cellzonation and suppressed angiocrineWnt-signal-ing.

• Due toadecreaseof canonicalWnt-signaling inhepatocytes metabolic liver zonation was dis-turbedandlivergrowthwasdecreased.

• Malignant melanoma cell adhesion and subse-quentmetastaticburdenintheliverwasreduceduponendothelialNotchactivation.

W186

Downregulation of VEGFR3 signalling mod-ifies cardiac lymphatic vessel network and reduces survival after MI

Taina Vuorio1,EliasYlä-Herttuala1,JohannaPLaakkonen1, Svetlana Laidinen1, Timo Liimatainen1,SeppoYlä-Herttuala1

1A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland

• Downregulation of VEGFR3 signalling in trans-genicsVEGFR3miceandChymiceledtoamodi-fiedcardiaclymphaticvesselnetwork.

• Attenuated lymphangiogenesis in sVEGFR3micepredisposedtohighermortalityaftermyocardialinfarction.

• Novel MRI methods, TRAFF2 and TRAFF4 revealedamodifiedstructureofinfarctionscarinsVEGFR3 mice.

W187

Hippo signaling effector Yap regulates hyaloid vasculature regression in the developing eye

MasahideSakabe1,YoshiOdaka1, Richard Lang1, Mei Xin1

1Cincinnati Children’s Hospital, Cincinnati, United States

• The Hippo signaling pathway regulates theregressionofhyaloidvessels

• Cellular translocation of Yes associated protein(Yap),aHipposignalingeffector,iscrucialfortheregression process

• TheHippo signaling pathwaymodulates hyaloidvesselregressionbypromotingcellsurvival

W188

The hallmarks of human DR are efficiently reproduced in novel retinopathy mouse model

Seiji Yamamoto1,HideyukiKitahara1,SayakaKajikawa1, Erika Azuma1, Takeru Hamashima1,YokoIshii1, Hikari Sato2, MasabumiShibuya3,MasakiyoSasahara1

1University of Toyama, Toyama, Japan, 2Tokyo General hospital, Tokyo, Japan, 3Jobu University, Gunma, Japan

• Novelretinopathymousemodelisgenerated• PDGFsignalisinvolvedinretinaldetachment• VEGF signal is involved in pathological angiogen-

esis

W189

A Novel Necrosis Inhibitor in Myocardial Ish-emia-Reperfusion Injury

Han Mo Yang1,Ju-YoungKim1,In-ChangHwang1, Sahmin Lee2, Joo-Eun Lee1, Joonoh Kim1,Hyo-SooKim1

1Seoul National University Hospital, Seoul, South Korea, 2Asan Medical Center, Seoul, South Korea

• Novelnecrosisinhibitor(NecX)markedlyreducedmyocardial I/R injury in comparison with CsA,vitaminC,andacombinationofvitaminCandE.

• The necrosis inhibitor significantly preventednecrotic cell death through the inhibition ofmPTPopening.

• In vivo, pretreatment with the necrosis inhibi-tor resulted ina significantly smallermyocardialinfarctsizethanCsAortheantioxidants.


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W190

Dll4 signaling maintains blood-retinal barrier integrity

Jee Myung Yang1,TaeWookNoh1,ChanSoonPark1, Soo HyunKim1, Injune Kim1

1Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea

• Dll4 inhibition induces reversible barrier disrup-tioninadultretinavessels

• Dll4signalingmaintainslowrateoftranscytosis.• Dll4/Notch signaling controls hypertension-in-

ducedBRBdisruption.

W191

Aortic lymphatic vessel: for or against athero-sclerosis in experimental models?

Kim Pin Yeo1,ChungHweeThiam1,CindyMeowLingPhua2,JoshuaP.Scallan3, Chi Ching Goh2, Dr. Jackson Lee2, MrWeiQiangSee1,MsYaTang1, Mr Xuan Hang Koh1, HweeYingLim1,SamanthaChew1, Lai Guan Ng2, Michael J Davis4,VeroniqueAngeli1

1National University Of Singapore, , Singapore, 2Singapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Biopolis, , Singapore, 3Department of Molecular Pharmacology and Physiology, University of South Florida, , USA, 4Department of Medical Pharmacology and Physiology, University of Missouri, , USA

• Atherosclerosis• Lymphaticfunction• LOymphangiogenesis

W192

5-Methoxytryptophan protects against arterial injury by promoting endothelial regeneration and smooth muscle cell differentiation

Shaw-fang Yet1, Chung-Huang Chen1,Yen-ChunHo1, Hua-Hui Ho1, Cheng-Chin Kuo1,KennethK.Wu1

1National Health Research Institutes, Zhunan, Taiwan

• 5-Methoxytryptophan attenuates endothelialdenudation-inducedintimalhyperplasia.

• 5-Methoxytryptophan protects against intimalhyperplasia via concerted actions of enhancingendothelialregenerationandpreservingdifferen-tiatedphenotypeofVSMCs.

• 5-Methoxytryptophan is a valuable therapeutictargetforarterialinjury-inducedvascularremod-eling, such as restenosis.

W193

Deletion of VEGFR1 in SMCs caused delayed retinal vasculature development, reduced alveolarization and myometrial thickness

Xiangke Yin1, Lijuan Huang1,LixianLiu1, Qishan Chen1, ZhiminYe1, Ran Liu1, Rong Ju1, Xuri Li1

1State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Guangzhou, China

• SMC-specificVEGFR1conditionalknockout(cKO)mice were generated to investigate the role ofVEGFR1expressedinsmoothmuscle;

• Delayed retinal vasculature development,reducedalveolarizationandmyometrialthicknesswereobservedinthemutantmice;

• VEGFR1playsdistinctiverolesinSMCscomparedto those in endothelial cells.

W194

Novel dual inhibitors of VEGF and PDGF receptors suppress ocular neovascularization via multitargeted effects

Xiangke Yin1, Xiangrong Ren1, Qishan Chen1,LixianLiu1, WeisiLu1, Xuri Li1

1Zhongshan Ophthalmic Center,Sun Yat-Sen University, Guangzhou, China

• TheseresultsindicatethatDAVP2andDAVP3dis-playhigherefficacythanVIDorPID2insuppress-ingocularneovascularization.

• DAVP2 and DAVP3 inhibit both HUVEC andHUVSMC migration and proliferation, whichmight stem fromsuppressingVEGFR2andPDG-FRβactivation.

• DAVP2andDAVP3arenovelpotentialtherapeu-tic drugs to treat ocular neovascularization dis-eases.


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W195

Pericyte-derived Dickkopf2 regenerates dam-aged penile neurovasculature through an angiopoietin-1-Tie2 pathway

Guonan Yin1,fellowMin-JiChoi1,StudntKalyanGhatak1, NguyenNhatMinh1,JiyeonOck1,Mi-HyeKwon1, Kang-Moon Song1,HeonJooPark2, Ho Min Kim3,Young-GuenKwon4,Ji-KanRyu1,5,Jun-KyuSuh1

1National Research Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, Incheon, South Korea, 2Hypoxia-related Disease Research Center, Inha University College of Medicine, Incheon, South Korea, 3Graduate School of Medical Science and Engineering, Korea Advanced Institute of Science and Technology (KAIST), Daejeon, South Korea, 4Department of Biochemistry, College of Life Science and Biotechnology, Yonsei University, , South Korea, 5Inha Research Institute for Medical Sciences, Inha University College of Medicine, Incheon, South Korea

• Dickkopf2(DKK2),aWntantagonist, isknowntopromote angiogenesis.

• Overexpression of DKK2 in diabetic miceenhances penile angiogenesis and neural regen-erationandrestoreserectilefunction.

• DKK2-mediated juxtacrine signaling in peri-cyte-endothelial cell interactions promotesangiogenesisandneuralregenerationthoughanangiopoietin-1-Tie2pathway

W196

The Phenotypic And Functional Properties Of Mouse Yolk-Sac-Derived Embryonic Macro-phages

Nejla Yosef1,TegyVadakkan1,June-HeePark2,RossPoché1, Jean-Leon Thomas2,MaryDickinson1

1Department of Molecular Physiology & Biophysics, Baylor College Of Medicine, Houston, United States, 2Department of Neurology, Yale University, New Haven, United States

• Flow cytometric isolation of yolk-sac-derivedembryonicmacrophages (EMs) fromCsf1r-EGFPtransgenicmouseembryos

• EMs possess pro-angiogenic and pro-inflamma-torypropertiesdistinctfromadultmacrophages

• EMshavegreatercapabilitiestodifferentiateintomicroglia as compared to adult macrophages when co-culturedwithmouse neural stem/pro-geintor cells

W197

TNF-α enhances TGF-β–induced endotheli-al-to-mesenchymal transition in endothelial cells by augmenting both TNF-α and TGF-β signals

Yasuhiro Yoshimatsu1,2,3,NaoyaTakahashi2, Kentaro Maeda3,KazukiYoneyama3,KoheiMiyazono4, Tetsuro Watabe2

1Department of Cellular Physiological Chemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical And Dental University, Tokyo, Japan, 2Section of Biochemistry, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan, 3Laboratory of Oncology, School of Life Sciences, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan, 4 Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan

• MolecularmechanismbywhichTGF-β and TNF-α cooperatively accelerate endothelial-to-mesen-chymaltransition(EndMT)

• TGF-βenhancesEndMTbyupregulatingitsrecep-torexpressionandtheavailabilityofitsactivatedform of the ligand

• TNF-α enhances its own signal in an autocrinemanneraswellasTGF-β signal

W198

Reticulon 4B is a novel regulator of macro-phage foam cell formation and atherogenesis

XinboZhang1, Cheng Zhang2,YaruCui2,YingyingLuo2, Jun Yu1,2

1Vascular Biology and Therapeutic Program, Yale University School of Medicine, New Haven, United States, 2Center for Metabolic Disease Research, Temple university Lewis Katz School of Medicine, Philadelphia, United States

• Reticulon 4B (Nogo-B) inhibits atherogenesis byattenuatingfoamcellformationandmacrophageapoptosis.

• ModifiedLDLactivatesMEKK3/JNK2/c-Junsignal-ingpathway,andc-JundirectlyactivatesNogo-Band SR-AI.

• Upregulated Nogo-B interacts with MEKK3 andmodulate foam cell formation through negativefeedbackontheMEKK3/JNK2pathway.


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W199

FGFR signaling-dependent Metabolic Regula-tion of Vascular Development

Pengchun Yu1, Michael Simons1

1Yale University Cardiovascular Research Center, New Haven, United States

• Fibroblast growth factor receptor (FGFR) sig-naling is critical for blood and lymphatic vesseldevelopment.

• FGFR signaling promotes endothelial glycolysisthrough controlling the expressionof the glyco-lyticenzymehexokinase2(HK2).

• FGFR signaling activation increases the expres-sionofMYC,whichdirectlydrivesHK2transcrip-tion.

W200

Hippo pathway in valve development and dis-ease

Wei Yu1, Bin Zhou1, Lei Zhang1

1Shanghai Institutes for Biological Sciences, Chinese Academy Of Science , Shanghai, China

• Vgll4ismainlyexpressedinheartvalves• Vgll4knockoutleadtoVICoverproliferationand

form thicken valve• SemiknockoutYaprescuedheartfromvalvemal-

formationinVgll4CKObackground.

W201

Bcar1/p130Cas is required for heart develop-ment and outflow tract septation in a trans-genic mouse model

MarwaMahmoud1, Ian Evans1,MissLauraWisniewski1, PaulFrankel1, Ian Zachary1

1University College London, , United Kingdom

• Conditional knockout of Bcar1 in early smoothmuscle cells and cardiac progenitors, using the SM22-Cre line, (Bcar1SM22KO) is lethal from embryonicday(E)13.5-14.5.

• Bcar1SM22KOembryosexhibitdefectivemyocar-dialisationandfailureofoutflowtractseptation,anddisruptedexpressionofproteins involved inepithelial-to-mesenchymaltransformation.

• Ourwork reveals a cell-specific requirement forBcar1inearlymyogenicandcardiacprogenitors.

W203

Modulation of PDGFR signaling at the blood brain during neuroinflammation

Manuel Zeitelhofer1, Milena Zeitelhofer Adzemovic1, ChristineMössinger1,ChristinaStefanitsch1, Tomas Olsson2, Linda Fredriksson1, Ulf Eriksson1, Ingrid Nilsson1

1Karolinska Institutet, MBB, Vascular Biology, Stockholm, Sweden, 2Karolinska University hospital, Neuroimmunology Unit, Stockholm, Sweden

• BBBisreactingdifferentlyinthepreclinical,pro-gression and remission phase of experimentalautoimmuneencephalomyelitis(EAE)

• BBB leakage and down-regulation of tight junc-tion components during the progression phaseandcanberescuedbyblockingPDGFR

• InterferingwithPDGFRsignalingdown-regulatesendothelial cell activationat theBBB leading toimprovedBBBintegrity

W204

Cell-autonomous and non-cell-autonomous roles of VEGFR3 in lymphangiogenic sprout-ing

Yan Zhang1, Maria Ulvmar1, Lukas Stanczuk1, Ines Martinez-Corral1,MaikeFrye1, Kari Alitalo2, Taija Mäkinen1

1Uppsala University, Department of Immunology, Genetics and Pathology, Uppsala, Sweden, 2Wihuri Research Institute and Translational Cancer Biology Program, Biomedicum Helsinki, University of Helsinki, Helsinki, Finland

• VEGFR3 is indispensable fortip lymphaticendo-thelial cell (LEC) function during embryonic andearly postnatal dermal lymphatic vessel sprout-ing.

• Early postnatal deletion of VEGFR3 causes lym-phatic hyperplasia by inducing proliferation ofnon-targetedVEGFR3+LECsthroughreductionofNotch signalling.

• Heterogeneity in VEGFR3 level drives vesselhyperplasia,providingimplicationsfortheunder-standing of mechanisms of developmental and pathologicaltissuegrowth.


– 169 –

IVBM2018

W205

Transient loss of integrity of developing veins causes RBC extravasation and clearance by lymphatic vessels

Yang Zhang1,NinaDaubel1,SimonStritt1, Taija Mäkinen1

1Department of Immunology, Genetics, and Pathology, Uppsala University, Uppsala, Sweden

• Transientlossofvenousintegrityduringdevelop-mental vascular remodeling

• Red blood cell extravasation and clearance bylymphaticvesselsindevelopingmesentery

• Plateletsmaintainvenousintegrity

W206

Targeting endogenous VE-Cadherin restores vascular integrity and facilitates the sub-set-specific modulation of leukocyte transmi-gration

Yang Zhao1, Jia Li1, Rohit Jain2,PaulColeman1, Ka Ka Ting1, JinbiaoChen3, Thorleif Moller4,WolfgangWeninger2, MathewVadas1,JenniferGamble1

1Centre for the Endothelium, Vascular Biology Program, Centenary Institute, the University of Sydney, Sydney , Australia, 2Immune Imaging Program, Centenary Institute, the University of Sydney, Sydney , Australia, 3Liver Injury and Cancer, Centenary Institute, the University of Sydney, Sydney , Australia, 4Mirrx Therapeutics A/S, , Denmark

• BlockmirCD5-2 isanoveloligonucleotide-basedinhibitor that specifically increases endogenousVE-Cadherinexpression,promotingbarrierinteg-rity.

• CD5-2 selectively regulates transmigration ofCD8+Tcellsandneutrophils.

• The balance between chemokines induced byCD5-2contributestotheselectivemodulationofCD8+Tcellandneutrophiltransmigration.

W207

A novel target of endothelial PKA regulates vascular sprouting by inhibiting Autophagy

Xiaocheng Zhao1,PavelNedvetsky1, Holger Gerhardt1,2

11Vascular Patterning Laboratory, Vesalius Research Center, VIB and Department of Oncology, KU Leuven, Leuven, Belgium, 22Max-Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Berlin, Germany

• Identified potential PKA substrates which maymediatetheeffectsduringangiogenesisthroughmassspectrometry(MS)andvalidatedsomeposi-tivePKAsubstratesintheMSlist.

• Identified PKA phosphorylation sites of its sub-strate ATG16L1 and PKA deficiency stabilizeATG16L1inbothHUVECandmicemodel.

• 3.Autophagy inhibitor chloroquine(CQ) partiallyrescued vascular hypersprouting and tip cellincreasing caused by inhibition of endothelialPKA.

W208

Human Type H Vessels are a Sensitive Bio-marker of Bone Mass

LiangWang1, Fei Zhou2,PengZhang1,YoujiaXu1,YingXu2

1Second Affiliated Hospital of Soochow University, Suzhou, China, 2CAM-SU Genomic Resource Center, Soochow University, Suzhou, China

• TypeHvessels (CD31^highEndomucin^High)arepresentinhumanboneswhichshowage-depen-dent decline.

• HumantypeHvesselscloselycorrelatewithbonestatusandcanbeusedasaearlybiomarker forboneloss.

• Desferrioxamine improves bone status viaenhanced angiogenesis in osteoporotic mice,indicating a potential target for improving bonequalityviainductionoftypeHvessels.


– 170 –

IVBM2018

W209

Development of an optogenetic system for endothelial specific Akt activation in vitro and in vivo

Wenping Zhou1,2, Emma Ristori1,3,4, Stefania Nicoli1,3,4, WilliamSessa1,2,3

1Department of Cell Biology, Yale University, New Haven, United States, 2Vascular Biology and Therapeutics Program, Yale University, New Haven, United States, 3Department of Pharmacology, Yale University, New Haven, United States, 4Department of Internal Medicine, Yale University, New Haven , United States

• ThisisthefirststudyapplyingAkt-targetedopto-genetics inendothelialcellbiologyandconnect-ingAktsignaldynamicswithECfunctions.

• Temporal Akt activation can be achieved usingthe developed optogenetic Akt system by con-trollinglightintensityandexposuretime.

• Lossof allAkt isoforms in zebrafishcausesmal-formationofdorsalarterybutnotcardinalveinorintersegmental vessel sprouts.

W210

Uncontrolled embryonic coronary angiogenic precursor expansion causes coronary artery anomalies in mice lacking Pofut1

YidongWang1,BingruoWu1,PengfeiLu1, Donghong Zhang1,ShwetaVarshney2, Gonzalo del Monte-Nieto3, ZhenwuZhang4,NicolasSibinga5, Ralf Adams6, Kari Alitalo7, RichardHarvey3,PamelaStanley2, Bin Zhou1

1Department of Genetics, Albert Einstein College of Medicine, Bronx, USA, 2Department of Cell Biology, Albert Einstein College of Medicine , Bronx, USA, 3Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Darlinghurst, Australia, 4Department of Medicine, Yale University , New Haven , USA, 5Department of Medicine, Albert Einstein College of Medicine, Bronx , USA, 6Max-Planck-Institute for Molecular Biomedicine, Münster, Germany, 7Wihuri Research Institute, University of Helsinki , Helsinki, Finland

• Coronaryangiogenicprecursorcellsexpresshighlevels of VEGFR3 and DLL4.

• POFUT1 regulates the DLL4/NOTCH1/VEGFA/VEGFR2signalingaxis,tocontroltheexpansionofcoronaryangiogenicprecursorcells.

• Excessive coronary angiogenic precursor expan-sioncausescoronaryarteryanomalies,leadingtomyocardialinfarctionandheartfailure.

W211

IKKβ and Wnt/β-catenin signaling interaction links inflammation to mesenchymal stem cell fate determination

YipengSui1,Se-HyungPark1, Joseph Fernandez2,PhilipKern1, Changcheng Zhou1

1University of Kentucky, Lexington, United States, 2Rockefeller University, New York, United States

• IKKβfunctions insmoothmusclecells (SMCs)toregulatevascularinflammationandatherosclero-sis development.

• Adipose progenitors express SMC markers, anddeficiency of IKKβ reduces adiposity and meta-bolicdisordersinhigh-fat-fedmice.

• IKKβ is a β-catenin kinase that regulates mesen-chymalstemcellfateinresponsetoovernutritionorinflammatorystimuli.

W212

Targeting ARF6, A Convergence Point For Multiple Pathways of Diabetic Retinopathy

Weiquan (wendy) Zhu1Department of Medicine, Program in Molecular Medicine, University Of Utah, Salt Lake City, United States

• ThesamesignalingpathwayutilizesdistinctGEFsto sequentially activate ARF6, and these GEFsexert distinct but complementary effects onVEGFR2traffickingandsignaltransduction.

• Targeting the small GTPase ARF6 alters VEGFR2trafficking and reverses signs of pathology in 4animalmodelsthatrepresentfeaturesofdiabeticretinopathyandinafifthmodelofocularpatho-logical angiogenesis


– 171 –

IVBM2018

W213

Laser Microdissection based compartmen-talization of tumor tissue is essential for microRNA profiling in drug development

Peter Jan Zwiers1,2,SusannaSkalicky3, Timara Kuiper1, MatthiasHackl3, Grietje Molema1,2

1University Medical Center Groningen, University of Groningen, Groningen, The Netherlands, 2Vivomicx bv, Groningen, The Netherlands, 3TAmiRNA GmbH, Vienna, Austria

• Small amounts of laser microdissected tumor and tumor vascular compartments are sufficient formicroRNAprofiling.

• microRNA profiling in small tissue samplesobtained by laser microdissection reveals pro-found difference inmicroRNA expression signa-tures betweenwhole tumor and subsets of celltypeswithinthetumor.

• Thiscombinationoftechnologiescanbeappliedto all stages of drug development.

W214

Characterization of the immune cell pools present in mouse and human atherosclerotic arteries.

Einari Aavik1, Tiit Örd1,MariaBouvy-Liivrand2, Kimmo Mäkinen3, Minna U. Kaikkonen1,SeppoYlä-Herttuala1,3,4

1A.I.Virtanen Institute, University of Eastern Finland, Kuopio, Finland, 2School of Medicine, University of Eastern Finland , Kuopio, Finland, 3Heart Center, Kuopio University Hospital, Kuopio, Finland, 4Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland

• Westudiedthevarietyofimmunecellspresentinatheroscleroticaortasofhyperlipidemicmiceandinhumanatherectomysamples.

• Phenotyping of immune cells by simultaneouscombining RNA transcriptomes and surface epi-topes of individual cells.

• We identified a surprisingly broad spectrum ofinflammatory and anti-inflammatory immunecellspresentinatheroscleroticarterialwallsam-ples of human and mouse origin.

W215

Mouse models for cell type-specific mRNA profiling: macrophage and smooth muscle cell transcriptomics in atherosclerosis

Tiit Örd1, Henri Niskanen1, Lari Holappa1,PetriMäkinen1, Mustafa Beter1, Miika Kiema1,IlyaSkovorodkin3, Susanna Kaisto3, Seppo Vainio3, Johanna Laakkonen1,SeppoYlä-Herttuala1,2,MinnaKaikkonen-Määttä1

1A.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Kuopio, Finland, 2Heart Center and Gene Therapy Unit, Kuopio University Hospital, Kuopio, Finland, 3Biocenter Oulu, Laboratory of Developmental Biology, InfoTech Oulu, Center for Cell Matrix Research, Faculty of Biochemistry and Molecular Medicine, University of Oulu, Oulu, Finland

• Genetically tagged ribosomes allow for affinitypurification of polysomal mRNA from a specificcelltypewithinatissuesample.

• We have introduced macrophage-specific andsmoothmusclecell-specificEGFP-taggingofribo-somesintotheLdlr−/−ApoB100/100atheroscle-rosis mouse model.

• Thesemouselineswillfacilitatecelltype-specifictranscriptional profiling, cell sorting and imag-ing inatherosclerosisandothervascularbiologystudies.

W216

RGS5 controls hypertension-induced RhoA activity in vascular smooth muscle cells

Caroline Arnold1, Eda Demirel1, Anja Feldner1, Guillem Genové3, Hangjun Zhang4,CarstenSticht2, Markus Hecker1, ScottHeximer4,ThomasKorff1

1Department of Cardiovascular Physiology, Institute of Physiology and Pathophysiology, Heidelberg University, , Germany, 2Center of Medical Research, Medical Faculty Mannheim, Heidelberg University, , Germany, 3Integrated Cardiometabolic Center, Karolinska Institute, Huddinge, Sweden, 4Department of Physiology, Heart and Stroke Richard Lewar Centre of Excellence for Cardiovascular Research, Toronto, Canada, 5Institute of Experimental and Clinical Pharmacology and Toxicology, Medical Faculty Mannheim, Heidelberg University, , Germany

• RGS5israte-limitingforRhoAactivityduringvas-cular remodeling in response to biomechanicalstress,i.e.hypertensionandarteriogenesis

• RGS5 deficiency prevents hypertension-inducedVSMCproliferationandthickeningofthearterialwall

• Loss of RGS5 increases Gαq/11-dependent PKCactivitywhichinhibitsRhoA

– 172 –

IVBM2018Author index

Author index

Aavik, Einari M175,W214Abdelilah-Seyfried,Salim M001, M048, M136Abdul-Salam,Vahitha W059,W060Abe,Takashige M190Ablooglu,Ararat W141Abramovich,Dalhia W011,W012Abshire,Caleb T109Abubaker,AishaAlsheikh W131Acker-Palmer,Amparo T112,W082Acker, Till T112,W082Adams, Ralf M007,M115,W210Adamski, Mateusz W100,W111Adinolfi,Simone T104Affolter,Markus M031Ager, Ann M170Aghi, Manish K. W081Aguzzi, Adriano T031Ahnströem,Josefin W016Aigrot, Marie-Stéphane T001Ainscough,Alexander W059Airavaara, Mikko M015Aird,William T205,W092,W161AitOufella,Hafid T086Aittokallio,Tero W061Ajtay,Kitti M002,W123Akkoyunlu,Nilay T177Al-Mardini, Claudia T163Alabrudzinska,Marta T006, T204Alakoski, Tarja M017Alarcon-Martinez,Luis M003Albarran-Juarez,Julian M004Albert,Anthony M188Albiges-Rizo,Corinne M001, M048, M136, T153Albäck,Anders T017Alencar, Adriana M. T154Alessandri, Kevin M013Alexandrescu,Sanda M036Alexandru,Nicoleta M005, M089Alexis,Josue W013Alhendi, Ahmad T034Alibert,Charlotte M156Alibrandi,Simona W079Alitalo, Kari M014, M015, M132, M169, M186,

T001, T008, T027, T063, T103, T190,T198,T210,W044,W064,W204,W210

Allan, David S. M139Allen,Lynsey-Dawn W018Almquist,Håkan W084Alonso, Florian M006Alt, Silvanus M158,W055,W183Altendahl, Marie M122Althoff,Till M004Alvarez-Aznar,Alberto M007, M063Alvarez-Buylla,Arturo W081Alve, Sanni E. M168

Alvino, Valeria W098Amado-Azevedo, Joana M198Ambartsumian,Noona W067Ameda, Kaname M190Amigo, Julio W144Ampuja, Minna M008Amram,Eytan W121Amrhein, Carolin M151Amudhala Hemanthakumar, Karthik

M009

Andaloussi Mäe, Maarja M010,M012,T179,W171Anderson, Deirdre T021Anderson, Georgina M219Andersson,Partrik M200Ando, Koji M011,M063,M144,W171Andrae, Johanna M012,W171Andreas,Martin M028Andriantsitohaina, Ramaroson

W159

Andrique,Laetitia M013Andrysiak,Kalina T023, T114Ang, Koon M184Angeli,Veronique M077,W191Anginot, Adrienne M177Angulo, Ana T129Anisimov,Andrey M014, T029Annex,Brian T032Antila,Salli M015, T001, T063Antoniali,Cristina W033Aoki, Junken M192Arany,Zolt T040Arima,Yuichiro T195Armesilla, Angel L M016Armstrong, Florence W031Arnal, Jean-Francois T086Arnold, Bernd T056,W182Arnold, Caroline T062,W216Arnould, Minh M048Arokiaraj, Mark Christopher

M018

Arora, Amita T061Arora,Shubhangi T167Arouche, Nassim M177, T115Artham, Sandeep W089Artiach,Gonzalo M060, M062Aryal,Binod T093Asaf, Lihee M019Aschacher, Thomas M028Asencio, Catalina W144Aspelund, Aleksanteri M015Asser, Toomas W133Atiya,Shahar W121Atli,Nursabah M105Augustin,Hellmut T044,T056,W093,W182Augustin,Iris T056Autio,MatiasIlmari M076

– 173 –


Avraham, Roi W136Avramut,Cristina W161Axelsson,Jonas M130Azuma, Erika W188Baaten, Constance C. W163Babataheri,Avin W137Babu,Mohan M020Bačáková,Lucie W145Badi, Ileana M021, T131Bãdilã,Elisabeta M005Bae, Hosung W006Bae, Jong Sup T102Bae, Jun Gu T042Bae,JungHyun M211Bae, Sun Sik M178, T099Baganha,Fabiana M022Baggott,RhiannonR M016Baig, Mirza M023Baillie,Gregory T060Bailly,Sabine M024, M108Baker,Andrew W077Baker,Andy M049Baker, Siân T210Bakker,ErikN.T.P. M025Balan, Mirela T204Balboa,Diego M008Balcer,Marly T138, T139Balint, Laszlo M026,W123Balistreri, Giuseppe M168Balland,Martial M136Ballmer-Hofer, Kurt W025Banfi,Andrea M027, M159Banham, Alison M184Baptista,Daniela M050Bar, Anna W111Barakat,AbdulI. W137Baranyi,Ulrike M028Barbee,Kenneth M035, T175Barreiro, Karina T017Barry,Mary M032Bartels-Klein, Eireen W183Bartels, Susanne W093Baruch, Amos W061Barwacz,Szymon T114Bassi, Ivan M029Bastos de Oliveira, Marta M030,W183Batchelor,TracyT. W081Bates, David T210Bats, Marie Lise M116Baudrie,Véronique W137Bauersachs, Johann M119, T054Baumann, Marc T029,W061Bayer,Carolyn T109Baylis,Richard T189Beck,HansKristian M101Beekman,Andrew M105Behrendt, Niels T198Bellmann,Lydia M120

Belting,Heinz-Georg M031Belton, Orina M032Benarab,Ammar T197Bender, R. Hugh F. M033Bendhack, Lusiane M128,W015,W033Bennett,Martin M061Bennett,Martin T002Bensimon-Brito,Anabela M042Bentley,Katie M147,M159,T215,W025Benyó,Zoltán M203Benzakour, Omar T018Berendschot, Tos M202Bergaya,Sonia M071Berger,Philipp W025Berger, Rolf T079Bergers,Gabriele M206,W176Bergman,Otto W119Bergmann, Sonja T208Bernhard, David M028Bertelli,PietroMaria W018Bertuzzi, Giacomo T179Besemfelder, Eva W093Bestholtz, Christer M010Beter, Mustafa T037,W215Bethani, Ioanna T112,W082Betsholtz, Christer M007, M011, M012, M063, M147,

M150, M195, T004, T168, T179, W052,W065,W171

Betteridge,Kai T210Betz, Timo M057Beyer,AndreasM. M034Bhattacharyya,Aparna M035Bhide, Mohit T040Bialas, Arkadiusz T114Bianchi, Marco M021, T131Bibli,Sofia-Iris M204,M205,W094Bichsel,Colette M036Biela, Anna T114Bieli, Dimitri Bieli M031Biessen, Erik M037,M146,W165Bijlenga,Philippe M111, T159Bikfalvi, Andreas M013, M038, M099Binet, François T144Bingley,John M219Bink,Diewertje M039,M040,W020,W109Birdsey,Graeme M041,M117,W016Biros, Erik M219Bischoff,Joyce M036Bjerkvig, Rolf M099, M162Blacher, Silvia T160,T198,W160Blaise, Regis W042Blanco,RaquelAgudo M159Blankensteijn, Jan D. M043Blinder,Pablo T191Bloksgaard, Maria M101, T141Bocchicchio,Sebastián M216Bochaton-Piallat,Marie-Luce

M058,M146,T159,W067

Boels, Margien W161

– 174 –


Boer, Christa M131Boettger,Thomas M054Boezio, Giulia LM M042Bogaard, Harm Jan T079,T134,W122Bogdan-Catrina, Sergiou T148Bogue,CliffordW M152Bogunovic, Natalija M043Boisserand, Ligia T001Boisson-Vidal, Catherine M112Bolton,Rebecca M044Bond, Gareth T188Bondareva, Olga W147Bonder, Claudine M045Bonfils,Gaëlle T142Bonnet,Sebastien T079Bonnin,Philippe T197,W137Boon, Reinier M039,M040,T071,T119,W020,

W109Bordenave, Jennifer M024Borén, Jan W061Borgolte, Julia M106Boscolo, Elisa M046Bot, Ilze M047Bou-Gharios, George T188Bouaboula,Mehdi T143Boulate, David T115Boulday,Gwénola M001, M048, M136Bouleti,Claire T138Bourgot,Isabelle T160Bourreau, Jennifer W137Boutin,Laetitia W031Boutros, Michael T056Bouvy-Liivrand,Maria T024,T078,T158,W214Bouzin,Margaux T191Bower,Mark M169Boyault,Cyril M136Boye,Kevin M038Boyle,JosephJ. M041Bracquart,Diane T089Bradshaw,AngelaCatherine

M049,M124,W077

Brakebusch,Cord M007, M063, M147Brambilla,Francesca M021Brand, Marjorie M139Brandt, Karim M050Brandt, Maarten M T117Brandt,Matthias M057Brash, James M044Braun, Laura M051Braun, Thomas M151Braunersreuther, Vincent T159Breazeale, Alec T121Breitkopf-Heinlein, Katja T056,T209,W182Bresciani, Jordan T149Brickman, Joshua M M152Bridges, Esther M184Britzen-Laurent, Nathalie T187Brkic, Sime M027Bronisz-Budzynska,Iwona T166,W027

Brorson, Håkan T027Brouard, Nathalie T014Brown,Markus W154Brown,Michael M045Bruche, Susann W099Bruikman, Caroline M160Brulois, Kevin M052Bruneau, Sarah M164Bruns,Alexander-Francisco

M053

Brüne, Bernhard W094Brzozka,Krzysztof T114Brännström, Johan M095, T207Buchegger, Bianca T145Buchroithner, Boris T145Buckner, Nicola T210Buczek,Elzbieta W100Bueno-Betí,Carlos W159Buerk, Donald T175Bui, Bang V. M092Burba,Ilaria M021Burger,Fabienne M050Burgisser,PetraE T117Burke, Aileen M174Bursill,Christina W045Busch, Karin W182Busch, Stephanie M183Busso, Dolores W012Butcher, Eugene M052Butler,Lynn M118Butz, Stefan M096, M179, M196Byskov,Kristina M054Byun,Jonghyun M210Bäck, Magnus M060, M062Caballero-Martinez,Amelia

M106

Cabe,Carolina M055Cadagan, David M016Cadenas, Vanessa M094Cadrouvele, Catherine M127Caetano, Bertrand W104Cagnone, Gael T215Cai,Yuqi M046Caines, Rachel M056,W148Caja, Laja M181Calado, Dinis M142Callahan,Abby T068Camerer, Eric M054,T197,W137Campillos, Mónica M001Candido, Juliana T171Canham, Maurice A M152Cannaert,Elyssa T122Cantelmo, Anna-Rita W161Cao, Jiahui M057,W178Cao, Xudong M084Cao,Yihai M200, T089Capogrossi, Maurizio C. M021Caporali, Andrea W098Caradu, Caroline W050

– 175 –


Cardoso dos Santos, Luis Miguel

M058

Cardoso, Cécile M048Carlantoni, Claudia M059Carlström,Mattias M060Carmeliet,Peter M107,M147,W161,W165CarracedoOrtiz,Miguel M060, M062Carrié, Didier T086Carriere, Catherine W108Carswell,Andy T149Cartland, Sian M061,W045Cartwright,ElizabethJ M016Casaletto,Kaitlin M122Casper, Janis M187Castro, Marco M063, M147Caulk,Alexander M071Cedervall, Jessica M064, M181, M189Ceffa,Nicolò T191Cerina, Manuela W166Cha,Howard T042Chan-Ling, Tai-Loi W139Chan, Mark M076Chan,YinTungCrystal M065, M066, M067, M068Channon, Keith M. W099Chapouly,Candice M069Chaqour,Brahim M125Charnaux,Nathalie T130Chatrou,Martijn M146Chau,Lee-Young M070Chaudhri,Reyhaan T180Chaussain, Catherine M112Chemtob,Sylvain T142Chen, Chung-Huang W192Chen, Hong M074Chen,Ivy W081Chen,Jinbiao W206Chen, Jun T060Chen,Pei-Yu M071Chen, Qishan M114,W193,W194Chen,Rongyuan M072Chen, Shou M132, T190Chen,Wei M151Chen,Xinyi M073Chen, Zehua M071Cheng, Caroline T117Cheng, Chao W108Cheng, Jianpin M169Cheng,WingKeungStephen

M065, M066, M067, M068

Chennupati,Ramesh M075, T106Cherepanova, Olga T032, T189Cheuk,LaiYeeBernice M068Cheung,Christine M076Chew,Samantha M077,W191Cheynier,Rémi M055Chiang, Ming-Tsai M070Chiba,Ayano M078Chichger, Havovi M079Chico, Tim T188

Chidiac,Rony T215Chignalia, Andreia Z W033Chilov, Dmitri M015Chioh, Florence M076Chirico, Giuseppe T191Chittenden,Thomas M071Chlopicki, Stefan T080,W035,W100,W111,W113,

W118Cho, Chang Sik T011Cho,Hyun-Jai T082Cho,Jeong-Hwan W005Cho,Youngkyu M080Cho,YunKyung T090Choe,Nakwon T081,W063Choi, Hong-Seok T012Choi,HyoungChul T047,W117Choi,JaesungPeter M081Choi,Jeongwoon M211Choi,Ji-Hyun M083Choi,Jiwon T042Choi, Kang Ho T048Choi,Kyu-Sung W003Choi, Mal-Gi T041Choi, Min-Ji W195Choi, Seung-Cheol M083, T200Choi,Seungbum M082Choi,YoungSun T102Chouleur,Tiffanie M038, M099Chouliaras, Kira M. T188Chrifi,Ihsan T117Christman, Karen L. M033Chronowska,Ewa W044Chrsitoffersson,Gustaf W022Chu, Alphonse M139Chu, Man M084Chung,Ju-Hye T049Chung,Minhwan T101Chung, Seok M080Church, Rachel T147Chuyun,Dimitry W121Cilfone, Nickolas M071Ciliberti,Giorgia M085Civelek, Mete M118, M134Claesson-Welsh,Lena M195, T010, T013, T118, T161,

W019,W052,W065,W095,W102,W177

Claria, Joan M060, M062Clark,Gabrielle T109Clarke,Murray T002Clay,Denis W172Cleaver, Ondine T110Cleuren,Audrey W162Cochrane,Amy M056,W148Cockshell, Michaelia M045Coen,Matteo M058Coleman,Paul M086,W139,W206Collini, Maddalena T191Collins, Kerrie M087Collins, Michelle M M152

– 176 –


Collins, Russil M030Commerford, Catharina T214Connor,Rebecca T149Constantin,Alina M005, M089Conze, Lei M090, M095Coornaert,Isabelle M091Cop, Florian T112,W082Coquoz,Oriana W106Corada, Monica T006Cordero, Eugenia T073Córdoba,Bernat W051Corniola, Marco T159Cosemans, Judith W165Cothran, Jonathan T178Coudert,Juliette W132Couedel- Courteille, Anne M055Couffinhal,Thierry M116Coultas, Leigh M092Coupland, Kirsten G. T208Couto, Ana M079Couty,Ludovic T197Cowin,Allison W138Coxam,Baptiste M093, M158Cramer, Louise T123Cresci,Barbara T170Croce, Kevin J M119Crocker,PaulR. M070Cruys,Bert M147Cruz-Crespillo, Ester M094Cubbon,RichardM W173Cuervo, Henar T178Cui, Long-Hui M083Cui,Yaru W198Cummings, Richard D. T214Cunha, Sara M090,M095,W149Currie, Silke M096,M157,W078Cutler, Daniel T123, T176Cybulsky,Myron W029Cysewski,Dominik M172Czarnowska,Elżbieta T080Czarny,Joanna W035Czyżyńska-Cichoń,Izabela T080D’Addio, Marco T214D’Alfonso, Laura T191D’Angelo, Rosalia W079d’Ario, Giovanni W105Daemen, Mat W165Dahl Bjørnholm, Katrine M097Dai, Jianing W093Dakhli,Thierry M006Dallinga, Marchien T052Dalloul, Rajja T113Damm, Miriam T112,W082Dancs,Peter M215Daniel, Jan-Marcus M119, T054Dantas,AnaPaula T203Das, Rudra M098Dasen, Boris M027,W021Daubel,Nina W205

Daubon,Thomas M038, M099Daudelin, Jean-François W180David, Sascha M100Davis, Michael J W191Davis, Sterenn T164Day,Robert W119DeBoer,Antina T138deBoer,Hetty T089,W169de Guire, Vincent W180de Koning, Eelco W161De la Salle, Henri T014DeMey,JoG.R. M101, T141DeMeyer,Guido M091, M102DeMoudt,Sofie M102De Munck, Dorien M102deMuylder,Bénédicte M055de Silva, Kevin W094De Val, Sarah T188de Vos, Judith M025de Vries, Carlie M103De Vries, Ingrid W154de Vries, Margreet M022,M104,W169DeWaard,Vivian M103deZúñiga,Ignacio W012De-Luca, Coralie M048Deak, Balint Andras M026Decante, Benoit T115DeCarli, Charles M122Deharvengt, Sophie W107,W108Deindl,Elisabeth M106Dejana,Elisabetta M063, M090, M095, T006, T207,

W175Dejda, Agnieszka T144,T215,W180Dekker, Nicole M131del Monte-Nieto, Gonzalo W210Delisle, Chantal T215Demandt, Jasper M107,W165Demirel, Eda W216Demory,Alexandra T056,W182DePinho,RonaldA. W179Dequiedt,Franck M037Deroanne, Christophe T198Derry,Brent M001Derszniak,Katarzyna W100Desideri, Sara T210Desroches-Castan, Agnès M024, M108Destaing, Olivier M136Detmar, Michael T214,W177Detter,Matthew M109Devraj, Kavi M110, M205Dharaneeswaran,Harita T040Dhaun, Neeraj W137DiPolo,Adriana M003Di Tacchio, Mariangela M110Diagbouga,Mannekomba M111, T159Dias, Nuno W084Diaz, Noelia W147Dibner,Charna M058Dickhoff,Chris W122

– 177 –


Dickinson,Mary W196Dierick, France T177Dierkes, Cathrin M142, M196Dieterich, Christoph T119Diett,Miriam T209,W182Dight, James W014Dimberg,Anna M064,M155,M189,T120,W164,

W175Dimmeler, Stefanie M039,M040,M151,T119,W020,

W109Disch, Frans T089Dizier, Blandine M112Dkhissi,Fatima T018Do,EunKyoung M201Dobrovolskaya,Irina W032Dobrzyn,Pawel M148Docherty,Craig T149Doi, Takefumi T205,W092Domenga, Valérie W043Domingues, Alison M112Donato, Luigi W079Donovan,Prudence W014Dooley,Steven T209Dorfmüller,Peter T115Dos-Santos-Luis, Damien T089Downes,Nicholas M113Dowsett,Laura M170, T164Dragan, Emanuel M005Dragomir, Anca M064Draijer, Richard M105Drakos, Stavros M151Drees, Dominik M179Drehmer, Diana W148Du,Yuxiang M114Dubé,KarinaN. W099Dubey,Olivier M200Dubois,Olivier W060Dubrac,Alexandre M115Duez, Catherine W104Dufourcq,Pascale M116Dufton,Neil W016,M117Duhamel, Marie M206,W176Dulak, Jozef M172,T023,T114,T166,W027,

W142Duncker, Dirk J T117Dunkel, Johannes W124Duplàa, Cécile M116Dupuy,Nicolas T159Durré, Tania T198Dusart,Philip M118Dutzmann, Jochen M119, T054Dziumbla,Sarah M085, M205Ebarasi,Lwaki M130Ebert,Lisa M045Ebroin,Marie T160,T198,W160Eckly,Anita T014Economopoulou,Matina W054Egaña,Isabel W025Ehrlich, Marek M028

Eichin, Dominik M120Eichmann, Anne M015,M115,T001,T206,W137Eklund, Lauri M121, M123, M180, T022, T038Ekvärm,Elisabeth W025El Bernoussi, Lamiaa T177El-Mansi,Sammy M049,M124,W077Elahi,Fanny M122Elahy,Mina T034Elamaa, Harri M121, M123, T038Elaskandry,Menna M125Elbasani,Endrit M169Eleftheriou,Nikolas T073Elgheznawy,Amro T084Eli,Yona M019Elima,Kati M129Ellmark,Peter M155Emanuel, Anna M126Enard,Wolfgang M163Endo,Hayato M143Engelbrecht,Eric M192Engelhardt, Stefan W064Engelholm, Lars T198Eom,GwangHyeon T081Eriksson,Per W046,W119Eriksson, Ulf M130, M138, M141, T148, T193,

W203Eringa,Etto M126,W152Erne,Paul W021Erpicum,Charlotte T198Espedal, Heidi M099Essand, Magnus M155,W022,W175Essers, Jeroen M103Esumi, Chiharu T195Etscheid, Michael M054Eurola, Solja M008Eussen, Simone M202Evans, Ian W201Evaristi,MariaFrancesca M127Eymery,Mathias M001, M048Fabritius,Matthias W034Fadel, Elie T115Fagerberg,Linn M118Fahning, Bernah M128Fair-Mäkelä, Ruth M129Faizullina, Dinara M171Fakhouri, Fadi M164Falkevall, Annelie M130, T148, T193Fan, Xuejiao W128,W129Fang, Shentong M009, M015, M132, M186Fang,Yun M133, M134Farahani, Navid M135Faurobert,Eva M001, M048, M136, T153Favara, David M184Favre, Julie M075Feige,Jean-Jacques M108Feldner, Anja T062,W216Femel, Julia M189, T121Feng, Jun M137Fernandez-Borja, Mar T067

– 178 –


Fernandez-Hernando, Carlos

M071, T093

Fernández, Esther W051Fernandez, Joseph W211Ferratge, Segolene M177Ferraz, Mariana S. A. T154Ferrer, Jorge M041Ferri,Debora M021Feyeux,Maxime M013Filip, Anna M148Filippi,Alexandru M089Filippova, Maria M027Filppu,Pauliina T088Fischer, Andreas W135Fisher,Edward M071Fisslthaler, Beate M126,W094,W112Fleming, Ingrid M126,M204,M205,T084,W094,

W112Fletcher, Evan M122Flister, Michael M034Floren, Michael T134Folestad, Erika M138Fonseca-Alaniz, Miriam H. T154Foo, Roger M076Foster,Rebecca T210Fotaki,Grammatiki M155Fournier, Laure T143Fraga-Silva, Rodrigo M050Fraineau,Sylvain M139Franco, Claudio A. M140Frankel,Paul W201Fransen,Paul M102Fredriksson, Linda M141,T193,W110,W203Frej, Cecilia W120Frey,Jasmin T214Fritzsche,Martin T188Frunza,Sabina M005Fruttiger,Marcus M218, T173Frye,Maike M142,W204Ftizsimons,Stephen M032Fujii,Nobutaka T173Fujii,Tomoyuki W090Fujita, Misato M143Fukuda, Nana M152Fukuhara, Daisuke W019Fukuhara, Shigetomo M011, M144Fukumoto, Moe M145Fukushima,Yoko T173Funatsu, Risa W092Funk,RichardHW W054Funken, Dominik W034Furmanik, Gosia M146Furuno, Kenji M182Furuyama,Tatsuo M145Fälker, Knut M167G.K., Rajanikant T070Gachet,Christian T014Gadeau,Alain-Pierre W050Gaengel,Konstantin M007, M063, M147, M150

Gaetani,Roberto M033Gaitantzi,Haristi T056, T209Galezowski,Michal T114Gallione, Carol M109Gallo, Angela M151Galvani,Sylvain T197Gamble,Jennifer M086,W139,W206Gamez Mendez, Ana T093Gamez, Monica T210Gan, Ana-Maria M148Gancz, Dana M149Gao, Erhe T103Gao, Fei W089Gao, Lin T050García-Caballero,Melissa W160Garcia-Collado, Maria M150García-Martín,Ana T124Gastaud, François T014Gatsiou, Aikaterini M151Gauvrit,Sébastien M152Gayral,Stéphanie T086,W042Gdula, Anna M154,W085Ge,Yun T102Gebala,Véronique M158Geczy,Carolyn M061Geerts, Dirk T067Gengenbacher,Nicolas W093Genner,Scott M061Génot,Elisabeth M006Genové, Guillem T168,W056,W216Gentry,Kaylee T109Georganaki, Maria M155George,Jestin M170, T164George, Steven C. M033Georgescu, Adriana M005, M089Georgiadou, Maria M156Gerasimovskaya,Evgenia T116Géraud,Cyrill T056,T209,W182,W185Gerecht, Sharon T126Gerhardt, Holger M030, M093, M158, M159, T138,

T139,W055,W183,W207Gerke, Heidi W124Germain, Stéphane T136Gerschütz,Rebekka M157Geudens, Ilse M158Ghatak,Kalyan W195Ghigo, Alessandra W042Ghosh, Chandra M100Ghosh, Mitrajit W081Gianni-Barrera,Roberto M027, M159Gijbels,Marion W165Gil,HyeaJin T110Gilad, Dan W121Gille, Anne-Sophie T143Gillies, Mark W139Gilmore, Brian F T146Ginsburg,David W162Girard,Jean-Philippe W132Giraud, Antoine W022

– 179 –


Gisterå, Anton W061Gladh, Hanna M138Glass, Rainer M162, M163Glémain,Alexandre M164Gnudi, Luigi T210Godoy,Alejandro.S W144Goebel,Max T020Goerdt, Sergij T056,T209,W182,W185Goertz, Ole W076Goessling,Wolfram T060Goetzl,Edward M122Goh, Chi Ching W191Goines, Jillian M046Gokina, Natalia T213Golledge, Jonathan M219Gomez Escudero, Jesus M166Gomez-DelArco,Pablo M016Gomez, Delphine M165Gondar, Renato T159Gonzalez Diez, Maria W046Gonzalez-de-la-Presa,Bernardino

W051

Gordon,Alexandra M069Gordon, Emma T013Gordts,PhilipL.S.M W140Gottgens,Berthold M041Goumans, Marie Jose T079,W122,W152Gramolelli, Silvia M168, M169Grando, Marcella M128,W015,W033Grant, Zoe M092Gratton,Jean-Philippe T215Graupera, Mariona T129Greenberg,Harry M188Greenwood,John M170, T164Greif, Daniel M. M115Grenegård, Magnus M167Grenier, Vanessa W180Grieve, David M056,W148Griffin,Erin M109Griffin,KathrynJ W173Griffioen,Arjan M189, M207, T052Griffith,Steven T189Grigorian, Mariam W067Grimes,William T123Grimm,Myriam M004Grishacheva,Tatyana M171Griveau, Amelie W081Grochot-Przeczek,Anna M172Groene, Hermann-Josef W161Groisman,Alex W141Groppa, Elena M027, M159Grunler,Jacob T148Grunspan, Moshe M029Gryaseva,Irina W101,W114Grützmann,Robert W047Gu,Xiaowu T110Guber,Vera T215Gucciardo, Erika M173Guduric-Fuchs, Jasenka M174, T147

Guenou, Hind W172Guenther, Stefan M110, M151, M152Guido, Sara W079Guignabert,Christophe M024Guihaire, Julien T115Guihot, Anne-Laure W137Guillevic, Oriane W031Guillonneau, Xavier W137Guilluy,Christophe T136Guimbal,Sarah W050Gujja, Sharvari M071Gulcher,Jeffrey M071Gurzeler, Erika M175,W058Gustafsson, Sonja T168Gutierrez,Edgar W141Guzman, Camilo M031, M156, M180Göritz,Christian T108Ha, Guillaume M177,W172Ha, Jung Min M178, T099Hackl,Matthias W213Haddad, Oualid T130Hadoke,PatrickWF W137Haegerling, Rene M179Haertl, Ricarda T112,W082Haglund, Caj M169Hajmousa, Ghazaleh M183Hakanpää, Laura M180Hakovirta, Harri T064Halawaty,Hanna T130Halle, Olga W124Haller, Hermann M187Ham,Dongwoo T015Hamanaka,Robert M133Hamashima, Takeru W188Hambardzumyan,Dolores M162Hamidi, Anahita M181Hammes,Hans-Peter M183, M204, M205Hamouten, Adel W183Hamsten, Anders W046Han,Dongkyo W007Han,Jung-Hwa T046Hanada, Sanshiro T195Hankemeier, T. W039,W040Hannah,Rebecca M041Hansson, Emil T168Hansson, Göran K. W119Hara, Toshiro M182Harabayashi,Toru M190Harada,Yukihiro T182Haraguchi, Shogo T050, T155Hardy,Serge M038Harmsen,MartinC. M183, T072Harrington,Elizabeth M137Harris, Adrian M184Harvey,Natasha M142Harvey,Richard W210Hatanaka,Yutaka M191Hauer,Christian W105Hauschild,Robert W154

– 180 –


Hautaniemi, Sampsa M168, M169Hautero, Olli T064Havenga, Menzo W077Havet, Chantal W104Hayashi,Yumiko T036, T172He, Chunrong M185He, Hao W093He,Liqun M010, M012, M130, M142, T168,

W171He,Yulong M084,W006He, Zheng M092Heck,Tommy W167Hecker, Markus T062,W216Hedin, Ulf M118,W020,W046,W062,W084,

W119Heemskerk,JohanW. W163Heidler, Juliana T084,W094Hein, Irina W155Heinolainen, Krista M186Heinäniemi, Merja T024, T078, T196Heiskanen, Emmi T104Heldin, Carl-Henrik W149Helenius, Mikko T116Helker,ChristianSM M042Hellberg,Carina W025Helle, Emmi M008Heller Sahlgren, Benjamin M130Helley,Dominique T143Hellman, Lars M189Hellström, Mats W025,W102Helmke,Alexandra M187Hemanthakumar Amudhala, Karthik

W064

Hen, Gideon M029Heng,ChewKiat M076Henrion, Daniel M075,W137Henry,Ronald M202Henzler, Thomas T056Hermenegildo, Carlos T203,W159Hernández de Sande, Ana T024, T078Hernández-Romero, Diana T019Herre, Melanie M064, M189Herrera Hidalgo, Carmen W022Herts, James T180Herzog,Wiebke T188Hess, Daniel T032, T189Heutschi, Daniel M031Hewer,Ekkehard T124Heximer,Scott W216Hibender,Stijntje M103Hida,Kyoko M190, M191Hida,Yasuhiro M190, M191Hierck, Beerend M111Higashiyama,Shigeki T067, T186Hillebrands,Jan-Luuk W103Hilvo, Mika W061Hinds, Monica T021Hinman, Jason M122Hirano, Naoki M143

Hirano, Satoshi M191Hirsch, Emilio T086,W042Hisano,Yu M192,W120Hla,Timothy M192,T135,W120Hla,Timothy T197Ho, Hua-Hui W192Ho,Yen-Chun W192Hoareau-Coudert, Bénédicte

T177

Hodivala-Dilke,Kairbaan M166, T171Hoffman,Matt M034Hofma, Benjamin W138Hofmann,Patrick M039,M040,W020Hogan, Benjamin M. M031, T060Hokkanen, Krista M193,W140Holappa, Lari T037,W215Holfinger,Irene W055Holl, Daniel T108Hollfinger,Irene W183Hollier,Pierre-Louis W050Hollmén, Maija W124Holm, Lena W022Holm, Maren M051Holmgren, Lars M209Holnthoner,Wolfgang M194Holst,Jeff M045Holzer,Martin W034Holzner, Silvio W076Hong,HyunSook W023Hong,SeonPyo W006Hong, Soon Jun M083, T200Honkura, Naoki M195,W052,W065Hope, Michael J. W123Hoppe, Esther M196Hoppensack, Anke M197Hordijk,Peter M131, M198, T067, T128Horng, Sam M069Horowitz,Arie M199Hosaka,Kayoko M200Hosman, Anna.E T089Hou, Mengzhuo M162Houben,Alfons M202Hovingh, Kees M160Hricisák, László M203Hsu, Bang-Gee T075, T076Hsu,Yaw-Wen M070Hu, Jiong M204, M205Hu, Junhao W093Hua,Yichao M206Huang, Hua M155Huang, Jianhua T167Huang, Lan M036Huang, Lijuan M114,W193Huang, Ru-Ting M133Huertas, Alice M024Hughes, Christopher M033, M208Hugues, Stephanie T069Hui, Lijian W093

– 181 –


Huijbers,ElisabethJ.M. M189, M207Huillard, Emmanuelle W081Hulmi, Juha T103Hultgren, Nan M208Hultin,Sara M209Humbert,Marc M024Humbert,Marion T069Humphrey,Jay M071Hutterer,Evelyn M209Huusko, Jenni M175,T190,W061Huusko, Tuija W068Huveneers, Stephan T129HwanChang,Young T121Hwang,Byungtae W004Hwang,In-Chang W189Hwang,Yoonha T157Hwang,Young T016Hytönen,Jarkko T064Hyun,Hoon T048Hyun,Sangho M210Hyvönen,Maija T088Häfele, Verena W185Hägerling, Rene M196Hätinen,Olli-Pekka M212Iba,Tomohiro M213, T172, T181Icay,Katherine M168Iftakhar-E-Khuda,Imtiaz M129,W126Ihara, Dai T183Ihugba,JudeC M016Ilmonen, Henna M214, T037, T085Imhof, Beat W106Inagaki,Shinobu M145Inagaki, Tadakatsu M217Inagawa,Toshihiko M218Inoue, Asuka M192Inuabasi,Linda M117Inverso, Donato T191,W093Ipe, Ute T201Iring, Andras M004, M215Irmukhamedov, Akhmadjon

M101, T141

Irtyuga,Olga T066Irusta, Griselda M216Irwin,AndrewJames M124Ishiba,Ryosuke W092Ishibashi,Tomohiko M217Ishii, Shuhei T183Ishii,Yoko W188Isidor, Nathalie T159Itakura,Yoko W072Itoh, Fmiko M218Itoh, Susumu M218Ivaska, Johanna M156, M168, M180, T216Iyer,Vikram M219Izawa,Kohei T205Izquierdo-Alvarez,Alicia W087Jabronka,Nikolett M203Jacak,Jaroslaw T145Jackstadt, Rene-Filip M170

Jacob,Laurent T001Jacobs,Stefan T204Jacquemet,Guillaume M156, M180, T116, T216Jahangiri, Arman W081Jain, Rakesh K. W081Jain, Rohit W206Jaisser, Frederic W111Jakus, Zoltán M002,M026,W123Jalkanen, Sirpa M120,M129,T116,W124,W126Jamalpour, Maria T105Jaminon, Armand T002,W163Jang, Cholsoon T040Janiak,Philip M127Janovicz, Anna M203Jansen, Erik W161Jaron, Dov T175Jaspard, Béatrice M116Jaszai, Jozsef W054Jasztal, Agnieszka W100Jauhiainen,Matti T029,T104,W061,W140Jauhiainen, Suvi M212, M214, T003, T085Jayaraman,Padma-Sheela M152Jazwa-Kusior,Agnieszka W142Jeanningros,Sylvie M116Jeansson, Marie M014, T004Jeffery,Steve T028Jeltsch, Michael M132,T005,T008,W044Jemelin, Stephane W106Jensen, Nina T006Jeon, Noo Li T055, T092, T100, T101Jeon, Seeun W007Jeong, Geon T081,W063Jeong, Jae-Hoon W091Jeong,Jin-Young T041Jerafi-Vider,Ayelet T007Jessup,Wendy M061Jha,Sawan T008,W044Jiang, Kai W093Jiang,Xiaoyi M179Jilishitz, Irina T135Jim, Kinki K. T128Jimenez, Connie J W152Jimenez,Wladimiro W051Jin, Han M107,W165Jin,SeoYeon M178, T099Jin,Suk-won T009Jin,Yi T010,W102Jin,Young-June T106Jinyu,Li M115Jo,DongHyun T011Jo, Hanjoong M039Jo,HyeRam W091Joe,Young-Ae T012Johansson,Staffan W175John, Gareth M069John, Liam T213Johnson, Randall W022Jokitalo, Eija M173Jones,ElizabethA.V. T013

– 182 –


Joo,HyungJoon M083, T200Joore, J. W041Jorge-Peñas,Alvaro W087,W167Jost, Camille T014Joung, Hosouk T081Joung,Hyojee T015, T016Jouppila, Annukka T017Joussaume, Aurélie T018Joutel, Anne W043Jover, Eva T019,W098Joyal,Jean-Sébastien T215,W180Jozkowicz,Alicja M172,T023,T114,T166,W027,

W142Ju, Rong M114,W193Jukema,Wouter M104Jukkola, Jari T022Jula,Antti W061Jun,Ho-Wook T095Jun,Yesl M080Jung, Chang Hee T090Jung, Cholomi T095Jung,YooJin M178, T099Jung,YunJi T127Juni, Rio T020Jura, Jolanta T080Jurney,Patrick T021Jägersberg,Max T159Kaakinen, Mika M123, T022, T038Kaarniranta, Kai T104Kabara,Maki T097Kachamakova-Trojanowska,Neli

T023,W142

Kaczara,Patrycja M172,T080,W113Kaczor,Dawid W100Kaempf,Andy T121Kahn, Mark L. M002Kaijalainen, Seppo T198Kaikkonen-Määttä,Minna M020, M113, M175, T024, T037,

T078, T085, T087, T111, T158, T174,T196,W086,W140,W143,W214,W215

Kaisto, Susanna T025,W215Kaivanto, Elisa M169Kajikawa,Sayaka W188Kakko, Sakari W068Kalaria, Raj N. T208Kallenberg,David M170, T164Kalliokoski, Kari T064Kalna, Viktoria M041,M117,W016Kamei,Yoshiaki T186Kameishi, Sumako M209Kamps, Jan W103,W146Kang, Dong-Hoon T012Kang, Hojin M087Kang, Li T102Kang, Min-Sook T016Kang,Sang-Won T012Kang,Sang-Wook W005Kang, Seok W006

Kang,SooHyun T102Kang,YuMi T090Kanitz,Alexander T027Kansanen, Emilia T104Kanse, Sandip M. M054,W034Kanthou,Chryso T018Kapiainen, Emmi T038Kapustin,Alexander M146Karaman, Sinem M015, M186, T027Karampatzakis,Alexandros M155Karapouliou,Christina T028Kareinen, Ilona T029Karginov, Andrei M087Karikó, Katalin W123Karikoski, Marika W124Karlsen, Tine Veronica W049Karlström, Helena T208Karlöf, Eva W084Karppinen, Sanna-Maria W182Kartawidjajaputra,Felicia M105Karttunen,Tommi T059Kasaai, Bahar T013Kashio, Taito W092Kataru, Raghu T030,W048Katayama-Kinugasa,Yumi T182Kaufmann,Walter W154Kaunisto, Aura M155Kavurma,Mary M061,W045Kawabata,Kenji T205Kawabe,Jun-ichi T097Kawakami,Koki M192Kawamura,Teruhisa T182, T183Kay,Colin M105Kazenwadel,Jan M142Kearney,MarkT. M053Keep, Richard F. T193Kelaini, Sophia M056,W148Keller, Annika M010,T031,T179,W074,W153Kelly-Goss,Molly T032Kelly,Daniel M049,W077Kempe, Birgit M157Kentala, Henriikka T061Kerimi, Asimina W151Kerkelä, Risto M017, M123, T103Kern,Philip W211Keränen, Sara M214, T085Kesavan, Rushendhiran M085Kessler, Hosrt T171Ketelhuth, Daniel FJ W061Kettunen,Sanna T033,W140Khachigian, Levon T034Khandoga, Andrej W034Kholová, Ivana T035, T217Khomich, Tamara W035Khosrotehrani, Kiarash W013,W014Kidoya,Hiroyasu T036,T172,W150Kiefer, Friedemann M142, M179, M196Kiema, Miika T037,W215

– 183 –


Kieronska, Anna W100,W111Kietadisorn,Marchy M037Kiflemariam,Sara T161Kihlström, Minna M121, T038Kij, Agnieszka T080Kikuchi, Hiroshi M190Kilimann, Manfred W065Kilpiö, Teemu M017Kim-Kaneyama,Joo-ri T050, T155Kim, Boa T040Kim, Do-geun T041Kim,DongYoung T043Kim,Dongkyu T045Kim, Eunjoon T043Kim, Ho Min W195Kim,Hyemi W007Kim,Hyo-Soo T082,W189Kim,Hyun-Kyung T012Kim,Hyung-seok T048Kim, Il-Kug T098Kim, In San T102Kim, Injune T057,T098,T199,W190Kim, Jae Ho M201Kim, Jaetaek T039, T081, T090Kim, Jeong Hun T011, T101Kim, Jeong-A T012Kim,JinHyoung T011Kim, Jong-Ho M083, T200Kim, Joonoh W189Kim, Ju-Hee T057Kim,Ju-Young W189Kim, Koung Li W116Kim,KyunHoo T044Kim, Mi Jin T041Kim, Minah T042Kim, Mirim T091Kim, Nacksung T081Kim,Pilhan T096, T157Kim, Se-Hong T049Kim, Seo Ki T045Kim, Seong-Ah T016Kim, Seul Gi T047,W117Kim,Shin-Hye W010Kim,SooHyun T199,W190Kim, Suji T046Kim, Sujin T046Kim,Suryong T092Kim,YooHyung M211Kim,Young-Kook W063Kim,Young-kuk T081Kindler, Diana T031Kinnunen,Kati T059Kirschenbaum,Daniel T031Kiss, Elina M180Kitahara,Hideyuki W188Kitajewski,Jan T135, T180Kitajima, Maiko T212Kitchen,Philip M152

Kittilä,Tiia W061KIvelä, Annukka T061Kivelä, Riikka M008,M009,T027,T103,W064Kiviniemi, Vesa T022, T051Klaassen,Ingeborg M183, T052Klapproth,Kay T056,W182Klaus-Bergmann, Alexandra

W183

Kleinert, Eike M106Kleinjan,Matthew T135Klems, Alina W109Klimovich, Vladimir W101,W114Klingler, Anika T187KlitgaardPovlsen,Gro M097Kloepper, Jonas W081Klohs, Jan T031, T053Klomp, Jennifer M087Kloska, Damian M172Kloss, Frederik M119Knoepp, Kai T054Knox,Jessica M001Knuuti,Juhani T064Ko, Jihoon T055, T092Ko, Nga Ling T213Koay,YenChin M061Kobayashi,Isao M144Koch,Philipp-Sebastian T056,T209,W182,W185Kockx,Maaike M061Koh, Bong-Ihn T057Koh,GouYoung M211,T044,T045,W006Koh, Xuan Hang W191Kohler,Sebastian M202Kohlstedt, Karin W094Koistinen,Hannu W044Koivunen,Peppi T058Kokki, Emmi T059Koltowska,Kaska T060Komorova,Yulia T135Kondadi,PradeepKumar W061Kondo, Kanako M145Kong, Eunji T096Koning, Jasper J W152Kono, Mari M192, T197Kontarakis, Zacharias M059Kontos, Christopher T146, T167Kook,Hyun T081,W063Koolwijk,Pieter T020Kopacz, Aleksandra M172Koponen, Annika T061Koppinen, Tapani M015Korff,Thomas T062,W216Korhonen, Ani M173Korhonen, Emilia M014, T063Korhonen, Vesa T022Korpela, Henna M212Korpisalo-Pirinen,Petra M027Korpisalo,Petra T064,W184Korsgren, Olle W022

– 184 –


Korte, Laura M119, T054Korth, Ruth-Maria T065Kostareva, Anna T066Koster, Annemarie M202Kostidis,Sarantos W161Kostina,Aleksandra T066Kotlinowski,Jerzy T080Kovačević,I. T128Kovacevic, Igor M198, T067Kovács,Gábor W123Kovala, Tom T068Kovanen,Petri T029,W061Kowalski,Camille T069Kozakowska,Magdalena T166,W027Kozhikkadan Davis, Charles

T070

Kramer, Joel M122Kraszewska,Izabela W142Krause,Matthew M134Kremer, Veerle T071Krenning, Guido M183,T072,W103Kridelka, Frederic W160Krieger, José T154,W105Krishna,Smriti M219Krishnan, Shanmugarajan W081Kritharides, Leonard M061Kritikou,Eva M047Krivchenko, Aleksandr M171Krombach,Fritz W034Kroon, Steven T089Kros, Johan M T117Kruczek, Szczepan T114Krutetskaia, Irina W101,W114Kubis,Nathalie T197Kubota,Yoshiaki M211,T057,W006,W125Kuiper, Johan M047Kuiper, Timara W213Kuipers, Jeroen M183Kuivanen,Antti M212Kukkonen-Macchi, Anu M129Kum,HyeJin M178, T099Kumar, Anil T074Kumawat,Ashok T219Kuo, Cheng-Chin T077,W192Kuo, Chiu-Huang T075, T076Kuosmanen, Suvi T078Kupp,Robert W081Kurakula,KondaBabu T079Kurata, Kaori T173Kurian, Leo W109Kurihara, Hiroki W127Kurpińska,Anna W118Kurusamy,Sathishkumar M016Kurzejamska,Ewa T073Kus,Edyta T080Kus, Kamil W111Kuster, Diederik T020Kwak,Brenda M111, T159Kwak,Shin M151

Kwapiszewska,Grazyna W088,W096Kwon,Duk-Hwa T081,W063Kwon,Hayan T127Kwon,Hyouk-Bum W109Kwon,Ja-Young T127Kwon,Mi-Hye W195Kwon,Yoo-Wook T082Kwon,Young-Guen T043,T083,W003,W195Künzel S.E., M115Künzel S.H., M115Kürschner,SinaWietje W182Kyselova,Anastasia T084Käkelä, Reijo W061Kälin, Roland M162, M163Laajala, Teemu Daniel W061Laakkonen, Johanna M214,T003,T037,T085,W186,

W215Laakkonen,Pirjo T088Laakso, Hanne M020,W140Laakso, Markku W058,W086,W143Laaksonen, Reijo W061Labrecque,Nathalie W180Lacolley,Patrick T150Laffargue,Muriel T086,W042Lagendijk, Anne K. M031, T060Laguna-Fernandez, Andrés M060, M062Laham-Karam,Nihay M113, T087, T174Lai,Yu-Hsien T075, T076Laidinen, Svetlana W186Laine, Anssi M175,W058Laitakari, Anna T038Laitinen,Mika T103Laitinen,Tomi T064Lakkisto,Päivi M017Lamandé, Noël T089Lambrechts,Diether W176Lane,Ryan T121Lang, Marie W016Lang, Richard W187Langer, Victoria W047Langhans, Claus-Dieter T056Lanza, François T014Lappalainen, Jari T037, T104Lappalainen, Kimmo M214Larivée, Bruno T215Larrouquere,Louis W081Larsson, Anders M064Larsson, Erik M064Larsson,Jimmy W025Lasch, Manuel M106Lassila,Riitta T017Lataillade,JeanJacques W031Lau,HweeHui M076Lauber,Kirsten W034Laufer, Günther M028Laurila, Juha M120Lautz, Thomas M106Laviña,Bàrbara M063,M147,M195,W052Lawrence,Anna-Lisa T193

– 185 –


Lawrence,DanielA. T193,W110Lawrence,Dylan T109Lay,Angelina M086Lazzaroni, Sharon M219Le Bloas, Rozenn M164LeBras,Alexandra W104LeGall,Sylvain M054Le Joncour, Vadim T088leNoble,Ferdinand W109Lebrin,Franck T089,W161Lee-Rueckert, Miriam T029Lee,ByungJoo T011, T101Lee,Byungjun T055, T092, T100, T101Lee, Choong-Kun W006Lee, Chunsik M072Lee, Eujin T097Lee,Eunhyeong T098Lee,HyeSun M178, T099Lee, Jackson W191Lee,jaeyeon T091Lee, Jingu T096Lee, Joo-Eun W189Lee,Junyeop T039Lee,Minkyoung M031Lee, Monica T093Lee, Sahmin W189Lee,Sandy T001Lee, Sang-Mok T011Lee, Sangmi M125Lee, Seok Jae T011Lee, Seung Eun T090,W007Lee, Seung-Jun W006Lee,Seung-Woo T012Lee, Seungjoo T098Lee, Shin-Jeong T094, T095Lee, Somin T055, T092, T100, T101Lee,TaeWook M201Lee,WooJe T090Lee,YooLa T090Lee,YouMie T102Lee,Younggyun T055, T092, T100Leeper, Nicholas T151Lehti,Kaisa M168, M169, M173, T088Lehti,Satu T027Lei, Xiao-Feng T050Leibing,Thomas T056,W182Leithner,Alexander W154Lemeille,Sylvain M111Lemitre, Mathilde W137Lemmens,Robin T138Lengquist,Mariette W084,W119Lennartsson, Johan W149Lenoir, Olivia W137Leon, Céline M099Leonard, Elvin V. W147Leppänen,Veli-Matti M132Leptidis,Stefanos T168Lerche,Martina M156, M180

Lerchenberger,Maximilian W034Lesch,Klaus-Peter W021Leshchiner,Ignaty T060Leung,WaiSum M185Leurgans, Thomas M101Levesque,Mitchell T124Levonen, Anna-Liisa T003, T078, T104Lewandowski,SebastianA W110Lhermusier,Thibault T086Li, Demin M184Li,Guangxin M071Li, Jia W139,W206Li, Jian T040Li, Marcella T165Li, Min M162Li, Rui T106Li, Taotao M084Li,Wanhong T074Li,Weiping W093Li, Xian M046Li, Xidan T168Li, Xinping T153Li, Xiujuan M084, T105Li, Xuri M072,M114,T074,T107,W193,

W194Li,Yue T034Li,Yuhuang W119Li,Yuping M163Li, Zhilin M015, T063Licina, Marijana W106Lie,Eunkyung T043Liebner,Stefan M205Liimatainen, Timo M020,W186Lilja, Johanna M156Lim, Do-Sun M083, T200Lim,HweeYing M077,W191Lim, I-Rang T200Lim, Jungeun T100Lim,Yeong-Hwan W063Limon,Isabelle W042Lin, Jihong M204, M205Lin, Ruizhu T103Lin,Yu-Li T075, T076LinckGuimarães,Eduardo T108Lindahl, Björn T105Lindberg,OlleR. W081Lindner, Marcus M197LindquistLiljeqvist,Moritz W119Lindsey,Sarah T109Lingasamy,Prakash W133Linn, Jasmine M034Lisicki, Elisa M197Lisowska,Justyna M136Little,Robert M016Liu,Boxiang T151Liu, Jianping T168Liu, Ke T188Liu,Lixian W193,W194

– 186 –


Liu, Oscar M212, T111Liu, Ran W193Liu, Xiaolei T110Liu,Xiaoting W093Liu,Yuhong M137Ljungberg,Liza T219Llaó-Cid,Cecília T112,W082Lobo,Tatiana T113Loboda,Agnieszka T114,T166,W027Loeys,Bart T122Lohi, Jouko M214, T085Loirand, Gervaise T150Loisel,Fanny T115Lokki, Marja-Liisa W061Loo, Christopher T121Loot, Annemarieke E. W094Lopez-Maderuelo, Dolores M016Losenkova, Karolina T116Lottonen-Raikaslehto,Line T104Louis, Thomas T198Loukovaara, Sirpa M173LouzaoMartinez,Laura T117Love, Dominic T118Low,Emma M049,W077Lozano-Vidal, Noelia M039,T119,W109Lu, Li T193Lu,Pengfei W210Lu, Sizhou T165Lu,Weisi W194Luck, Bert W094Lugano,Roberta M155,T120,W175Lund, Amanda T121Luo,Yingying W198Luo, Zhengkang T105Lupieri, Adrien T086,W042Lutz, Sarah T135Luyckx,Ilse T122Ly,Catherine W048Lyck,Ruth T124Lykkesfeldt,Jens M097,W097Lähteenmäki, Hanna W061Lähteenvuo, Johanna M212,W064M.Martinez,Carlos T019Ma, Haisha W149Ma,Wanshu T110Maaninka, Katariina T029Macas, Jadranka M110Mach, François M050Macklin, Bria T126Madden, Thomas D. W123Madeddu,Paolo W098Madhavan, Ragaseema V M181Maeda, Kentaro W197Maegdefessel, Lars W084,W119Maekawa,Masashi T067Maeng, Seo Jin M178, T099Maeng,Yong-sun T127Maffia,Pasquale M047

Mager, Hans-Jurgen J T089Magga, Johanna T103Magnus, Svala W158Magnusson,Peetra M095, T207Mahan,Sidney M165Mahmoud,Marwa W201Mahon, Niall M032Maillard, Loic T130Maischein,Hans-Martin M152Maishi, Nako M190, M191Majolee, Jisca T067, T128Makinen, Taija M196, T137Malashicheva, Anna T066Malet, Nicole T086,W042Malette,FréderickAntoine T215Malik, Asrar M087Malinova, Tsveta T129Mallet,Christine M024, M108Mamoune, Hadjer T130Manca, Marco M037Mancinelli, Luigi M021, T131Manet, Sandra M136Mangsbo,Sara M155Mann,AlexanderW. T084Manneville,Jear-Baptiste M156Mansour, Sahar M179Manuneedhi Cholan, Pradeep

M061

Manz, Xue T134Mao,DeYu T135Marazzi, Giovanna T177Marcassoli, Guilia M091Marchand, Marion T136Marchuk, Douglas M109Marczyk,Brygida W111Mardinoglu, Adil T027Margariti,Andriana M056,W148MarinJuez,Ruben M149Marín-Juez,Rubén M152Marín,Francisco T019Marine, Jean-Christophe T139Marsch, Elke M107,W165Martello, Andrea W098Martin-Almedina,Silvia T028Martin,Ivan W021Martin,Kathleen M115Martin,Sabrina T089Martin,Scherzer M200Martinet,Wim M091, M102Martinez-Corral,Ines M142,M169,T137,W179,W204Martínez-González,José T019Martinez-Martinez,Sara M016Martinez,Gonzalo M061Martinez,MaríaCarmen W159Martins,Beatriz M173Martowicz,Agnieszka T006Maruyama,Satoshi M190Mas, Magali M055Masaki, Takeshi M217

– 187 –


Masiero, Masimo M184Masson,Justin W016Mastrella, Giorgia M162Mateuszuk, Lukasz T080Mathieson,Peter T210Mathivet, Thomas M015, T001, T138, T139, T197,

W137MaticPerisic,Ljubica W046Matsumoto, Ken T139Matsunaga,Yukiko T097, T140Matsuno,Yoshihiro M190, M191MatthewFielden,Matthew

M142

Matthies,Maximilian T141Mattila,Heli T051Mattos,AnaB.M. T154Mattot,Virginie T142,W104Mauge,Laetitia T143Mawambo,Gaëlle T144,T215,W180Mayr,Sandra T145McBride,Martin M049McClung, Joseph M T146McClure, John M049McCord,TimothyJ T146, T167McCormack, Jessica T123McDonald, Donald T042McLoughlin, Kiran W018McNeill, Brian M139Medina, Reinhold M174,T147,W018Mehlem, Annika M130, T148, T193Mehling,Matthias W154Mehrara,Babak T030,W048,W123Mehta,Shwetal W081Meier, Katja W055Mejia-Cordova, Mariela T105Melo, Joana T147Mena,Agustina W011Ménard, Catherine T215Mendrysa,SusanM. T081Meniel, Valerie S T187,W047Mennander, Ari T035, T217Mercer, John T149Mercier, Nathalie T150Mercier, Olaf T115Merentie,Mari T104Merkel, Susanne T187Mervaala, Eero M009, M180, T190Mesaeli, Nasrin T113Messner,Barbara M028Meunier, Michel W180Meyer,Mathias T056Miano, Joseph T151Micha, Dimitra M043Miinalainen, Ilkka M121, M180, T025Mikami, Kasumi T212Mikhailova, Irina M171Mikkola, Hanna M132MiklosNagy,Bence W088Mikula, Michal W027

Mikulski, Maciej T114Miles, John M219Miletic,Hrvoje M099Miller, Clint T151Miller,Kristin T109Mills, Stuart W138Miloudi, khalil T215Mimura,Nobuko W090Min,Elizabeth T152Min, Jeong-ki W004Minh,NguyenNhat W195Miroshnikova,Yekaterina M136, T153Misawa,Yukiko W090Missiaen, Rindert M206Mitjavila Garcia, Maria Teresa

W172

Mittmann,Laura W034Miura, Takashi T195Miyakawa,AyumiA. T154Miyamoto,Tatsuki M218Miyasaka,Masayuki M129,W126Miyauchi,Aya T050Miyazaki,Akira T050, T155Miyazaki,Takuro T050, T155Miyazono,Kohei W197Mizuguchi,Hiroyuki T205MIzuno,Yumi M182Mocci, Giuseppe T168Mochizuki, Naoki M011, M078, M144, T162, T184Moganti,Kondaiah M183Mohaissen, Tasnim W100,W111Mohr, Laura T112,W082Molema, G W146Molema, Grietje W162,W213Molinier,Brigitte M127Molitor,Martin W145Moller, Thorleif W139,W206Molthoff,CarlaFM W152Mompeon, Ana T203,W159Monnot, Catherine T136Montanez, Eloi M163,T156,W178Montassar, Fadoua W137Monteith,Corey M135Montgomery,Ruth M071Moon,HyeJi M201Moon, Jieun T157Moonen, Jan-Renier A.J. T072Moorlag, Henk W146Morales-Ruiz, Manuel W051Morawietz,Henning W054Moreau,Pierre T078, T158Morel, Sandrine M111, T159Morfoisse, Florent T160, T198Morgado, Suzanne M055Morgan, Claire W059,W060Mori,Hiroyoshi M217Mori, Motomi T121Morikawa,Masato W158Morimoto, Hirofumi M191

– 188 –


Morin, Eric T161Morita, Kazuki W090Morooka, Nanami T162Morrell, Nick M049Morsing,Sofia T163Mortimer,PeterS. M179Morton, Susan M219Moss, Stephen M170, T164Motta,Alexandre M105Motterlini,Roberto W113Moulton, Karen T165Moustakas,Aristidis M181Moxon,Joseph M219Mozes-Autmazgin, Ziv W121Mucha, Olga T114,T166,W027Muehleder, Severin M194Mueller, Sarah T167Muhl, Lars M138,T168,T193,W110Mui,BarbaraL. W123Mukhopadhyay,Debabrata(Dev)

T169

Mulder,Barbara M103Muller, Laurent T136Mummery,ChristineL T089MuñozFélix,JoseManuel T171Muñoz-Martín,Noelia M094Munshaw,Sonali W099Murakami, Akari T186Muramatsu, Fumitaka T036,T172,W150Muraro, Manuele M027Murata, Takahisa T173Murcott,Clare M016Murphy,Andrew M061Murphy,Dana M034Murtada, Sae-Il M071Mushimiyimana,Isidore T087, T174Musílková,Jana W145Musters, René T020Mutlu, Gokhan M133Mutryn,Marie T165Muzorewa,Tenderano T175Mühlbauer,Olivia M105Myllyharju,Johanna M123Myllylä,Teemu T022MyoMin,KayKhine M045Mäkelä, Tomi M156Mäki, Joni M123Mäkinen, Kimmo T064,W214Mäkinen,Petri M020,W215Mäkinen, Taija M142,M169,W179,W204,W205Mössinger,Christine T193,W203Na,Kyuhwan M080Nadaud, Sophie T177Nadeem, Taliha T178Naemura, Kazuaki W127Naessens, Daphne M. M025Nagamatsu, Takeshi W090Nagaraj, Chandran W088,W096Nagasawa,Takashi T173

Nahar,Khayrun M010,T179,W171Naiche, L. A. T180Naidansuren,Purevjargal T012Naito, Hisamichi M213,T172,T181,W150,W157Nakagawa,Osamu T182, T183, T205Nakajima,Hiroyuki T184Nakamasu, Akiko T195Nakamura-Nishitani, Tomoe

T183

Nakamura, Masaki M200Nakamura, Toru M191Nakano,Yota M218Nakaoka,Yoshikazu M217, T044Nakashima,Yasutaka M182Nakayama,Akiko M215, T185Nakayama,Hironao T186Nakazawa,Ayumi T186Nam,Hyo-Jung W002Nam,Yoonseok T081Namba-Hamano,Tomoko T173Nanda, Vivek T151Narmada, Balakrishnan Chakparani

M076

Naschberger,Elisabeth T187,W047Nash,Andrew M130, T148Nashimoto,Yuji T195Nassoy,Pierre M013Navrulin, Victor M148Neal, Alice T188Neal, Chis T210Nedvetsky,Pavel W207Néel, Mélanie M164Negrotto,Soledad W011Neidert, M. W074Nemecz, Miruna M005, M089Neuenschwander,Martin M001Neuhofer,Wolfgang T062Newman,Alexandra T189Neyses,Ludwig M016Ng, Lai Guan W191Nguyen-Ngoc,Kim-Vy M033Nguyen,Anh M165, T032Nguyen,SuDuy T029,T190,W061Ni,Ruiqing T053Niaudet, Colin M147Nicklin,StuartAnthony M124,W077Nicoli, Stefania T192,W209Nielsen,NisValentin M054Nieminen, Markku S W061Nieminen, Tiina T003Niessen,HansW W152Nieswandt,Bernhard M096Nightingale,Thomas T123Nigsch, Florian W105Niinimäki, Eetu T035Niiranen, Otso M168Nikpey,Elham W049Nilsson, Ingrid T193,W110,W203Nilufar, Sharmin M139

– 189 –


Ning, Chenfei T194, T204Nishida-Fukuda,Hisayo T186Nishida, Kohji W157Nishihara, Hiroshi M191Nishio, Hisanori M182Nishiyama,Koichi T182, T195Niskanen, Henri M175, T024, T037, T078, T087,

T174,T196,W140,W215Nitschké,Maximilian T042Nitzsche, Anja T197,W025Nivet-Antoine, Valérie M112Nivoit,Pierre W137Nizet, Jean-luc T160Noel, Agnes M037,T160,T198,W160Noh, Ji-Min T200Noh,TaeWook T199,W190Noordstra, Ivar W168Nordlohne, Johannes M187Nornes, Svanhild T188NorwoodToro,Laura M034Nossent,Yaël T071Nottebaum,Astrid M157Nottebaum,AstridFee T201Noueihed, Baraa T142Novella, Susana T203,W159Nowak-Sliwinska,Patrycja T052Nowak,Witold T166,W142Nuchel, Julian T129Nurmi, Harri M015, M132, T190Nyqvist,Daniel T006, T204Näpänkangas, Juha T104Nätynki,Marjut M121, M123O.Bernabeu,Miguel W183O. Dias, David T108O’Connor, Marie M170, T164O’Neill,Christina T147O’Sullivan, John M061O’Connell, Maria M105O`Neill,Christina W018Obad,Nina M099Obernier,Kirsten W081Oceandy,Delvac M016Ochendrowitsch,Melanie M216Ock,Jiyeon W195Ock, Sangmi T039Ocskay,Zsombor M026Odaka,Yoshi W187Odeberg,Jacob M118,W084,W119Offermanns,Stefan M004, M075, M119, M215, T106,

T185,W170Ogola, Benard T109Oguri, Eri M144Oh,Won-Jong T041Ohga, Shouichi M182OhlinSjöström,Elisabet W019Ohme, Julia M170Ojala,PäiviM. M168, M169Ojala, Tiina M008Okada,Yoshiaki T205,W092

Okazawa,Makoto M217Okuda, Kazuhide Shaun T060Okun, Jürgen G. T056Ola,Roxana T206Olauson, Hannes M130, T148Oldenburg,Joppe T207Oldham, Michael C. W081Olichwier,Adam M148Oliveira, Daniel V. T208Oliver, Guillermo T110Olkkonen, Vesa T061Olsavszky,Victor T056,T209,W182,W185Olschewski,Andrea W088,W096Olschewski,Horst W088Olsson, Anna-Karin M064, M181, M189Olsson, Tomas W203Olsson, Venla T059Olverling, Anna T193Omori, Keisuke T173Omoto, Tomokatsu T050OnbehalfofthePREINSUTtrialinvestigators,

T143

Onions, Karen T210Oranje,Paul M105Orriols, Mar T019Orsenigo,Fabrizio M209Ortega-Gomez, Almudena M151Ortega, Sagraria W123Ortsäter, Henrik M142Osaka, Mizuko T211Osanai, Tomohiro T212Osman, Ahmed W060Osol, George T213Ostergaard,Pia M142, M179, T028Ostrowski,Jerzy W027Osuna Almagro, Lourdes M041Otonkoski, Timo M008Otten,Cécile M001, M048Otto,VivianneI. T214Ouarné, Marie M108Oubaha,Malika T144,T215,W180Oubiña,Gonzalo W011,W012Oudar, Olivier T130Oudard, Stéphane T143Owens,Gary M165, T032, T189Oxendine,Michael T110Ozber,ClaireH W173Paatero,Ilkka M031, M168, T216Paavola,Jere M017Paavonen,Timo T035, T217Pabst,Oliver M129,W124Paccosi,Sara T170Padel,Thomas W056Padgett,Michael T167Paech,Jennifer W064Pagel,Judith-Irina M106Paiste,Päärn W133Pala,Laura T170Palii,CarmenG. M139

– 190 –


Palombo,Isolde M130, T148Pan,Jingxuan T218Pan,Xiaoke T134,W122Parades,Genaro M183Parborell,Fernanda W011,W012Pardi,Norbert W123Pardo,Heidy M109Parenti,Astrid T170Pari,AshikAhmedAbdul W093Parikh,Samir M100Parinot,Célia W180Park,ChanSeok T199,W008,W009Park,ChanSoon T199,W190Park,Cheol-Young T090Park,Chi-Yeon M083Park,HeonJoo W195Park,HyeRim W007Park,Intae W006Park,JaeHyoung W001,W002Park,JeongAe W003Park,Jong-gil W004Park,Jong-Tae T048Park,Joong-Yeol T039, T090Park,Jun-Hee M015Park,June-Hee W196Park,Kyu-hwan W005Park,KyungWoo T082Park,Man-Seok T048Park,Mi-Jung W010Park,Se-Hyung W211Park,WooJin T081Park,YongSeek W007Park,Yongdoo T091Park,Young-Hee T016Parkar,Ashfaq M127Parrilla,Marta T112,W082Party,Joris T140Pascuali,Natalia W011,W012Pasternack,Arja T103Patel,Jatin W013,W014Patel,Jyoti W099Patel,Sanjay M061Patella,Francesca T176Paterson,Scott T060Pathak,Varun W018Patrakka,Jaakko M130Paul,Gesine W056Paulo,Michele W015Paulsson-Berne,Gabielle W119Paulus,Walter T020Paupert,Jenny T198Pauty,Joris T097Pavoine,Catherine T177Pawelec,Paulina M148Payne,Sophie T188Peacock,HannaM. T013Pedrini,EdoardoPedrini M174Peghaire,Claire M116,M117,W016

Peghaire,ClaireR. M041Peiper,Amy M109Peirce,Shayn T032Peixoto,Elisa W018Pek,Nicole M076Pekkonen,Pirita M168Pelli,Graziano T159Pelttari,Saku T217Penninger,Josef M002Pereira,Helena T143Perez-Cremades,Daniel T203Pericleous,Charis W016PerisicMatic,Ljubica W020,W062,W084,W119Perkins,TheodoreJ. M139Perlmoter,Gal M149Perola,Markus W061Perovic,Tijana W183Perrin,Laurent M058PersicMatic,Ljubica M118Personic,Nicolas M172PerssonSkare,Tor W019Persson,AndersI. W081Perttunen,Sanni M017Perälä,Nina M168Pestel,Julliette T001Peters,Erna M022, M104Peters,Kevin M051Petrishchev,Nickolay M171Petrova,Tatiana M169,W065Pettersson,Knut M022Petzelbauer,Peter W076Pfister,Frederick M183Pham,Phat W020Phan,Carole M024Phayon,Paul T086Philippides,Andrew W025Philippova,Maria W021Phillips,JoannaJ. W081Phillipson,Mia T108,W022,W083Phua,CindyMeowLing W191Piao,Jiyuan W023Pichol-Thievend,Cathy T136Piechota-Polanczyk,Aleksandra

M172

Pietilä,Ilkka W024Pietilä,Riikka T038,W025Pietras,Kristian T073Pietraszek-Gremplewicz,Katarzyna

W027

Pihlajaniemi,Taina W182Pilon,Frédérique W180Pinchbeck,Jenna M219Pinte,Sébastien W104Pinto,Anna M036Pirinen,Eija T104Pitkäranta,Anne T085Pitter,Bettina W178Pjanic,Milos T151Plant,Karen T188

– 191 –


Planus,Emmanuelle M136Plate,KarlH. M110Plomann,Markus T129Plow,Edward W026Pluskota,Elzbieta W026Poble,Paul-Benoit M024Poché,Ross W196Podkalicka,Paulina T114,T166,W027Pohan,Grace T021Poirier,Bruno M127Poissonnier,Loïc T142Poittevin,Marine T197Polak,Dawid W028Polenz,Chanele W029Polizzotto,Andrea M021Pollenus,Thomas W030Polycarpou,Andreas M203Pompilio,Giulio M021Ponamarczuk,Halszka W085Ponsen,Anne-Charlotte W031Popa,Eliane W162Popielarski,Marcin W085Popov,Gury W032Popp,Rüdiger M204,M205,W112Popryadukhin,Pavel W032Porcelijn,Leendert T163Portolés,Irene W051Portörő-Gál,Piroska M203Potente,Michael W179Potje,SimoneRegina W033Poulet,Mathilde M038Prabhu,Saurabh M105Praetner,Marc W034Prasain,Nutan M139Proia,Richard M192, T197Proniewski,Bartosz M172,W035,W100Pronk,Manon M198, T067, T128Proudfoot,Diane M146Proulx,Steven W177Proust,Richard W031Provost,Bastien T115Pruniaux,Marie-Pierre M127Przyborowski,Kamil W100Przybyt,Ewa M183Przygodzki,Tomasz W028Puche,CarmenMaría T019Pujol,Nadege M013Pula,Giordano W131Pulkkinen,Heidi T037Qian,Junbin W176Qin, Lingfeng M071Qiu, Jiedong W103Qiu,Mei-Yu T045Quaggin, Susan M014, T004Quax,Paul M022,M104,W169Quertermous, Thomas T151,W062R.Aburto,María T112,W082Rabelink,Ton T089,W161,W169

Radaelli,Fabrizio T191Rademakers, Timo M037Radhamani Chandran, Rachana

M115

Rafaeva, Maria M156Raftrey,Brian W038Raimbault-Machado,Jessica

T177

Raimondi, Claudio W016Raitamaa, Lauri T051Rajaraman, Anusha M052Rajna, Zalan T051Rakipovski, Günaj M097Ramadurai, Dinesh K. A. M151Ramakers, C. W039,W040,W041Ramanujam, Deepak W064Rambow,Florian T139Ramel, Damien T086,W042Ramming, Andreas W047Ramms,Bastian W140Ramnath, Raina T210Rancez, Magali M055Randi, Anna M041,M117,W016Randriamboavonjy,Voahanginirina

T084,W094,W112

Rantakari,Pia W124Rantanen, Ville M169Rao, Deepak M071Ratelade, Julien W043Raucci, Angela M021, T131Rauniyar,Khushbu T008,W044Rautou,Pierre-Emmanuel W183Ravindran,Dhanya W045Raviv, Ifah M019Raymond,Karine T089Razuvaev, Anton W046,W119Recarti,Chiara T002Recher, Gaelle M013Redl, Heinz M194Redondo, Juan Miguel M016Redpath, Andia N. W099Regen,Tommy M151Regensburger,Daniela T187,W047Reginato, Silvia M027Regli, L. W074Regnault,Véronique T150Rehal, Sonia W048Reichel, Christoph A. W034Reichel,Matthias M189Reikvam, Tore W049Reiss,Yvonne M110Ren,Wuwei T053Ren, Xiangrong M072,W194Renault, Marie-Ange W050Renier, Nicolas T001Renné, Thomas M118Repo,Pauliina M168, M173Resink, Therese J. W021Retzlaff,Jennifer M100

– 192 –


Reutelingsperger, Chris M146,T002,W163,W165Reynaud,Annabel W050Rezende, Flavio Rezende T215Rho, Seung-Sik M144Ribeiro-Silva,JoaoC. T154Riber,LarsPeter T141Ribera,Jordi W051Ricard-Blum,Sylvie T136Richards, Mark M195,W052Richter, Anne W158Richter, Karsten W182Richter,Tobias W158Ridwan,Yanto M103Rieck,Kristy M139Rinaldi, Carmela W079Rippe, Catarina W062Ristori, Emma W209Ritso, Morten M139Ritter,Mathias T112,W082Ritvos, Olli T103Rivera, Jose Carlos T142RiveroMartín,Olga W021Robciuc,Marius T190,W064Robert,Florian M024Robertson,Stacy M061, M124Robinson,Christopher T123Roche,FrancisP. W019,W025Rodewald,Hans-Reimer W182Rodriguez-Arabaolaza,Iker W098Rodriguez-contreras, Adrian

W053

Rodriguez,Cristina T019Roediger, Ben M086Roeffaers,Maarten W167Rojo Arias, Jose Eduardo W054Rol, Nina W122Romani, Nikolaus M120Romanoski,Casey M134,W143Rondon Galeano, Maria T060Rorsman,Charlotte T207Rosa, Andre W055Rosenholm, Jessica T088Rossi, Andrea M059Rossi, Laura T068Rotella, Carlo,Maria T170Roth, Aline M050Roth,Lynn M102Roth, Michaela W056Rotllan, Noemi T093Rouillon, Camille T150Rovnaia, Aleksandra W057Rowitch,DavidH. W081Rowther,FarjanaB M016Roy,Joy W119Roy,Peter M001Rudel,Lawrence W061Rudnicki, Michael A. M139Ruegg, Curzio W106Ruehle, Frank M037

Ruehle,PaulF. M054Ruf,Wolfram T084Ruhrberg,Christiana M044Rundqvist,Helene W022Ruokamo-Korva, Katri W068Ruotsalainen, Anna-Kaisa T104,W058Rusin, Kinga T166Russomanno,Giusy W059,W060Ruuth, Maija T190,W061Ryan,Nicola M032Rykaczewska,Urszula W046,W062Ryu,Hye-Won T048Ryu,Ji-Kan W195Ryu,Juhee T081,W063Rzymski,Tomasz T114Räsänen, Markus T103,W064Rödel, Claudia M136Röhl, Samuel W046Saarma, Mart M015Sabo,JenniferK. W081Sacchi, Veronica M027Saccu, Claudio M021, T131Sadoine,Jérémy M112Saharinen,Pipsa M014, M168, M180Sahgal,Pranshu M156Saikin, Semion W141Sáinz-Jaspeado, Miguel M195,W052,W065,W177Saito,Yuki M218Sakabe,Masahide W187Sakai,Yasunari M182Sakaue, Tomohisa T067Sakic, Antonija W067Sakurai, Takashi T201Salles-Crawley,Isabelle W016Salmi, Marko M120,W124Salminen, Marjo M142Salminen,Päivi M214Salmon,Andrew T210Salonurmi, Tuire W068Saltzman,WMark T001Salvermoser, Melanie W178Salza, Romain T136Samén, Erik T193Samoylovich,Marina W101,W114Samus,Maryna W069Sanchez-Duffhues,Gonzalo

W122

Sanchis, Juan W159Sander, Maike M033Sandler, Stellan T105Sano, Kengo M218Sano, Masaki W070Sansom,Owen M170Sapieha,Przemyslaw T144,T215,W180Saqib,Uzma W071Sargis,Timothy T180Sasagawa,Tadashi W090Sasahara,Masakiyo W188Sasaki, Norihiko W072

– 193 –


Sassoon, David T177Satchell, Simon T210,W098Sato, Hikari W188Satta,Sandro W073Saupe, Falk M064, M181, M189Sauteur, Loïc M031Savage, Aaron M M016Savant,Soniya T108Savolainen, Markku W061,W068Sawatari,Natsuki T186Saygili,Cansaran W065Scaglioni, Dominic T176Scallan,JoshuaP. W191Schaenzer, Anne W082Schaffenrath,J.B. W074Schaller, Karl T159Schaper, Nicolaas M202Scharinger, Bernhard M028Schaubächer,Johanna W034Schellerer, Vera S T187Scherzinger, Aaron M179Schiffers,Paul T002Schimmel, Lilian W168Schledzewski,Kai T056,T209,W182,W185Schlierbach,Hannah T112,W082Schlingemann, Reinier T052Schmid, Benjamin W047Schmid,Bettina W178Schmid,ChristianDavid T209Schmidt, Harald M146Schneider,Martin W075Schneider, Sven T056Schnittler,Hans M057,W147,W178Scholz, Johanna M197Schossleitner, Klaudia W076Schouten, Jan M202Schram, Miranda M202Schreiner,Bettina W153Schrimpf, Claudia M100Schulte-Merker, Stefan T060,W166Schultze, Joachim M155Schurgers, Leon M146,T002,W163,W165Schwab,Ursula W061Schwartz,Martin T152Schwartze,Julian M049,W077Schweda,Frank M075Schäfer,Kerstin M051,M096,M157,W078Schänzer, Anne T112Scimone,Concetta W079Scotney,Pierre M130, T148Scotti,Leopoldina W011,W012Seano, Giorgio W081Searcey,Mark M105Secondini, Chiara W106Sedding, Daniel M119, T054See,WeiQiang W191Segarra, Marta T112,W082Segerstolpe, Åsa T168

Seguy,Camille M116Seignez, Cédric W022,W083Seime, Till W046,W084Seki, Takahiro M200Sekiguchi,Kiyotoshi T162Sekine,Ayumi M024Sela,Yogev M019Selander, Tuomas T064Selkov,Sergey W101,W114Sellke, Frank M137Selmi, Anna M154,W085Selvarajan,Ilakya W086,W143Selzman, Craig H. M151Semenova, Daria T066Sennino,Barbara T042Sennlaub,Florian W180Seo, Ha-Rim M083Seo,Songyi W116Seol, So Mi T090Seppänen, Tapio T051Serné, Erik H M126,W152Sessa,William T093,W051,W209Seya,Daiki T183Shackleton, Mark M045Shafiee,Abbas W013Shah,AartiV. M041Shanahan,Cathy M146Shankman, Laura T189Shao, Zhuo W180Shapeti,Apeksha W087Sharma, Neha W088,W096Shashkova, Olga W101Shaw,Andrew M049Sheehan, Stehpen M032Sheldon, Helen M184Shelley,WilliamC. M139ShellyBen-Shushan,Rotem

W121

Shelton, Samuel J. W081Shen,Weiyong W139Shenoy,SomanathP.R. W089Shergill, Bhupinder M033Shi,Chenyue W179Shi,Guangbin M137Shi,Lingyan W053Shibuya,Masabumi W090,W095,W102,W188Shin, Jiae T015Shin, Sera W063,T081Shin,Young-Joo W091Shinohara,Nobuo M190Shirakura, Keisuke W092Sholapurkar, Radhika T188Sibinga,Nicolas W210Sidoti,Antonina W079Siegbahn,Agneta M181Siekmann, Arndt F W147Sihto, Harri T088Sihvola, Virve T104

– 194 –


Silanos, Andrea T131Silva, Naomi T042Silvente, Ana T019Silvestre,Jean-Sébastien W137Silvestris, Domenico Alessandro

M151

Sim, Seen-Ling W013,W014Simionescu,Maya M089SimoesDobrydnio,Laura M203Simons, Cas T060Simons, Karin M104Simons, Michael M071,W199Sindi,Hebah W059Singh, Kailash T105Singh,Sandhya T209,W182Singhal, Mahak W093Sinisalo, Juha W061Siragusa, Mauro W094Sirén, Juuso M017Sirisko, Mirja M119Sirois, Jacinth M038Sironi, Laura T191Sirsjö, Allan T219Sitarz, Kamil T114Sixt,Michael W154Sjollema, Klaas M183SjöbergHägerstrand,Elin W019Sjöberg,Elin T161,W095Sjöblom,Tobias T161Skalicky,Susanna W213Skofic-Maurer,Davor W088,W096Skovorodkin,Ilya T025,W215Skovsted,GryFreja M097,W097Slater, Sadie W098Sluimer, Judith M037,M107,W165Slütter,Bram M047Smadja, David M112Smart, Nicola W099Smeda, Marta W100Smeets, Harm M047Smirnov,Ilya W101,W114Smirnova, Natalia T086,W042Smith,JacquelineY. W108Smith, Jessica M053Smith,Kelly T060Smith, Ross W025,W065,W102Smits, Nicole W107Smulders,Yvo M126,W152Snijder, Repke.J T089Sodhi, Akrit M205Soehnlein, Oliver M151Sokolov,Dmitriy W101,W114Sol, Marloes W103Sol,Wendy M160,W161,W169Soleti,Raffaella W159Solinhac, Romain T086Solodovnikova,Nellya W101Sommer, Kathleen M110

Son, Dongchan T095Son,Kyungmin T101Son,Youngsook W023Soncin,Fabrice T140, T142Soncin,Fabrice W104Song, Eric T001Song, Eunjoo T157Song, Kang-Moon W195Song,Myeongjin T091Song,Sukhyun T045Sorensen, Ben M202Sorokin,Lydia W078Sotomayor,Paula W144Soubrier,Florent T177Sousa,Iguaracy W105Sowinska,Agnieszka T080Spencer-Dene,Bradley T056Spijkers, X. W041Spinetti,Gaia W098Spirito, Rita T131Spring, Kathleen M157Spronk, Henri M.H. W163Srun,Samly T089Staffaroni,Adam M122Stainier, Didier M042,M059,M149,M152,W109Stalin,Jimmy W106Stan, Radu W107Stan, Radu V. W108Stanchi,Fabio T138, T139Stanczuk, Lukas W204Stanicek, Laura T071,T119,W020,W109Staniczek, Theresa W182Stanley,Pamela W210Stasch, Malte M157Stasiak, Marta M154Stefanitsch,Christina M141,T193,W110,W203Stehouwer,Coen M202Stellos,Konstantinos M151Stelzmüller, Marie Teres M028Stemmer- Rachamimov, Anat

W081

Stenman, Ulf-Håkan W044Stenmark, Kurt T134Stenvinkel,Peter W084Stepniewski,Jacek T023Stergiopulos, Nicolas M050Stern,Christian M028Sternak, Magdalena W100,W111,W118Steuwe,Christian W167Sticht,Carsten T056,T209,W182,W216Sticht,Heinrich W047Stingl,Heike W112Stitt,Alan M056,T147,W018Stockmann,Christian T138Stoebener,Daniel M197Stoitzner,Patrizia M120Stojak, Marta W100,W111,W113,W118Stolbovaya,Anastasia W101,W114

– 195 –


Stoll, Monica M037Stone-Elander, Sharon T193Strilic, Boris M004, M152Stritt,Simon W205Struck, Eike M118Strudwick,Xanthe W138Struman, Ingrid W030StyevkónéDinnyés,Andrea

W123

Stürzl, Michael T187,W047Stöcklein, Veit M162Su, Enming T193,W110Su, Meiling W128Subramanian,Aishwarya T042Suh,Jun-Kyu W195Suh,Wonhee W116Sui,Yipeng W211Sultan,Ibrahim W064Sun,Hongye M071Sun, Lele M071Sundelin,Birgitta M130Sundell, Veronica M090, M095, T207Sung,JinYoung T047,W117Suraj, Joanna W118Sutter,Esther T159Sutton,Angela T130Suur, Bianca W046,W119Suuronen, Erik J. M139Suva, Mario L. W081Swart,Maarten M047Swendeman,Steven W120Swennen,Geertje T013Świątkowska,Maria M154,W085Swärd,Karl W062Symons,R.Andrew M092Synowitz,Michael M163Szabó,Zoltan M123, T103Szade, Agata M052Szafranska, Karolina T080Szőke,DánielImre W123Szpak, Dorota W026Szuchman-sapir, Andrea W121Szulcek,Robert T134,W122Szymborska,Anna W183Szymoński,Marek T080Säälik,Pille W133Taavitsainen, Jouni T064Tabaczar,Sabina M148Taccia, Filippo T131Tadayon,Sina W124Taddei, Andrea M142Taeri, Tofan T193Tai-Nagara, Ikue W125Taiwo,Adewale M168Takabatake,Yoshitsugu T173Takada,Yasutsugu T186Takagi, Takahiro M218Takahashi, Haruko T097

Takahashi,Naoya W197Takakura,Nobuyuki M213,T036,T172,T181,W150,

W157Takeda, Akira W126Takubo,Naoko W127Talar, Marcin W028Tallgren, Camilla T116Tam,YingK. W123Tan,Fuxing T218Tan, Joanne W045Tan, Lih M045Tanaka, Toru T182, T205Tang, Eva Hoi Ching M073Tang,Waiho W128,W129Tang,Ya W191Tanko,Gabriela M005, M089Taponen, Saija T103Tarafdar, Anuradha W131Tardiveau, Claire W132Tarjus, Antoine W111Tartour, Eric T143Tarvainen, Santeri T064Tarvainen, Tanja T064Taskinen,Marja-Riitta T027Taskinen,Panu W068Tatti-Bugaeva,Olga M168Taylor,Verdon M163Teesalu,Tambet W133Tellides, George M071Temitayo,Idowu M100Tempelhof, Hanoch W134tenDijke,Peter M049Tenkerian, Clara T187,W047Tenstad, Olav W049Teo, Adrian M076Tesone, Marta W012,M216Testini,Chiara T161,W025,W102Tetzlaff,Fabian W135Tevet,Yaara W136Thalgott,Jérémy.H T089Tharaux,Pierre-Louis W137Theelen, Thomas M107,W165Therattil,Anthony M069Therond,Patrice T197Thiam,ChungHwee W191Thibault,Guillaume T121Thiede, Bernd M054Thijssen, Victor L M189Thomas, Hannah W138Thomas, Jean-Léon M015,T001,W196Thorikay,Midori M049Thota, Durga Devi M020Thuillet, Raphaël M024Thöle, Janina W094Tiemeier, Gesa W161Tien, An-Chi W081Tikkanen, Ilkka M017Tillet, Emmanuelle M108

– 196 –


Timens,Wim W122Timmerman, Ilse M157Ting, Ka Ka M086,W139,W206Tirosh,Itay W081Tirronen, Annakaisa M193,T037,W140Tjomsland, Vegard T161Tkachenko, Eugene W141Tobiasova,Zuzana M071Toivanen,PyryI. T003,W140Tomczyk,Mateusz T166,W142Tomisawa,Toshiko T212Toropainen, Anu W086,W143Torres-Estay,Verónica W144Torres, Miguel M094Tournier-Lasserve, Elisabeth

M001, M048, M136

Toyoda,Masashi W072Tozuka, Minoru T029Trani, Marianna M027, M159Traver, David W141Trávníčková,Martina W145Trégouët,David-Alexandre M118Tremblay,Michel M038Trietsch, S.J. W039,W040,W041Trindade, Reginaldo Almeida

W146

Tripathi, Vineeta T164Troidl,Kerstin M106Tsai, Dong-Lin M070Tsaryk,Roman W147Tsifaki, Marianna M056,W148Tsioumpekou, Maria W149Tsujikawa,Takahiro T121Tsukada,Yohei T172,W150Tu,Ly M024Tucker,Rebecca T165Tuit, Sander M155Tukiainen, Erkki M214Tulamo, Riikka T017Tumova, Sarka W151Tuohinto, Krista M168, M169Turaihi,AlexanderH W152Turk,MaryJo W108Turunen,PauliinaS. T088Tuszynska,Irina T024, T196Tveden-Nyborg,Pernille M097,W097Türkcan, Adrian M028Török,Orsolya W153Uccelli, Andrea M027, M159Uchikawa,Michie T195Uemoto, Taiki T183Uemura,Akiyoshi T173, T195Uetani, Noriko M038Ugur, Milas M129Uhl, Bernd W034Uhlén, Mathias M118Ulbrich,Friederike T056,T209,W182Ulvila, Johanna M017Ulvmar, Maria W204

Umana, Claudia T136Uni, Kazumasa M145Uusitupa,Matti W061Uzan, Georges T115,W031,W172,M177Vaahtomeri, Kari W154Vaas, Markus T053Vadakkan,Tegy W196Vadas,Mathew M086,W139,W206Vaeyens,Marie-Mo W167Vafaeinik, Farzaneh M178, T099Vainio, Laura T103Vainio, Seppo T025,W215Valdés, Mariano T019Valdimarsdottir,Gudrun W158Valkama, Teemu M175,W058vanAgtmaal,Marnix M202vanBeijnum,JudyR. M207van Bezu, Jan M198, T128van Buul, Jaap T163,W168Van De Velde, Maureen W160VandeWelde,Maureen T160van den Berg, Bernard W161,W169vandenBorn,Jacob W103van den Brom, Charissa M131vanderEnt,Martijn W162van der Feen, Diederik T079van der Heijden, Thomas M047van der Kallen, Carla M202van der Sar, Astrid M. T128van der Velden, Jolanda M039, M040, T020van der Vlag, Johan W103,W161vanDijk,ChristianGM T117van Duijn, Janine M047van Duinen, V. W039,W040vanEys,Guillaume M146Van Gils, Janine M160van Gorp, Rick M146, T002Van Gorp, Rick H. W163vanHinsbergh,Victor M126,M198,T020,W152van Hooren, Luuk M155,M189,W164van Ingen, Eva T071van Kuijk, Kim M107,W165vanLeeuwen,Anoek M131vanLessen,Max W166van Meurs, Matjis M100Van Noorden, Ron T052van Oeveren-Rietdijk, Annemarie

W169

VanOosterwyck,Hans W087,W167vanPoelgeest,Erik M126Van Steen, Bram W168van Vught, R. W041van Zandvoort, Marc T002van Zonneveld, A.J. W039,W040van Zonneveld, Anton-Jan M160,W161,W169VanBavel, Ed M025Vanchin,Byambasuren T072Vanhoutte,Paul M185

– 197 –


Vanlandewijck,Michael M010,M012,T168,W065,W171Vaquerizas,JuanM W147Vara, Dina W131Vargas-Valderrama, Alejandra

M177,W172

Vargas, Diego A W087Varol, Chen M019Varshney,Shweta W210Vasileva, Margarita W101Vaughan,Andrew T123Vavilov,Valeriy W032Veerman,Krystle W132Vemuri,Kalyani T120,W175Vemuri,VenkataN.P. M135Venkatraman, Lakshmi W177Verboogen,DanielleRJ M189Vercesi, Juliana A W015,W033Vergori, Luisa W159Verhaar, Marianne C T117Verhamme,Peter T013Verkaik, Melissa M126Verstraeten, Aline T122Vessieres, Emilie W137Vestweber,Dietmar M051, M096, M157, M179, M196,

T201,W069,W078,Vidal-Gomez, Xavier T203Vihervaara, Terhi W061Vihinen, Helena M173Vihriälä, Erkki T022Vilà-González, Marta M056,W148Villafranca-Baughman, Deborah

M003

Villain, Gaëlle T142,W104Villasenor, Alethia M152Vincent,Pierre W042Vink, Hans W161Vion, Anne-Clémence M158,W183Vion, Elodie M139Virtakoivu,Reetta W124Vlaar,Alexander T163Vogels, Ilse T052Vogt, Ingo M001Volkery,Stefan M096,M157,W078von Kries, Jens M001VonVietinghoff,Sibylle M187Vonk,Alexander M131Vono, Rosa W098Vottero,Giulia T160Voutilainen,Merja M015Vreeken, Dianne M160Vulto,P. W039,W040,W041Vuola,Pia M214, T085Vuong,MinhP. T208Vuorio, Taina M193,W140,W186Vågesjö, Evelina T108,W022Vähä-Koskela, Markus M169Wagner,Helga W155Waisman,Ari M151Wakabayashi,Taku M213,T181,W157

Walczak,Maria W118Walker,AndrewMN W173Wallace,MarshaD. T188Walzog,Barbara M106,W178Wang,Chih-Hsien T075, T076Wang,Gangqi W161,W169Wang,Guilin M071Wang,Lei T106Wang,Liang W208Wang,Nancy W081Wang,Shasha M114Wang,ShengPeng M004,M215,W170Wang,Tina T151Wang,Weiguang M016Wang,Xiaomeng M170Wang,Xinsheng M200Wang,Yidong W210Wang,Zheng M071Wanga,Shaynah M103Warmke,Nele W173Watabe,Tetsuro W197Watala,Cezary W028Watanabe,Yusuke T182, T183Watkins,Thomas M219Watson,Angharad M170Weber-Stadlbauer,Ulrike T031Weigert,Andreas W094Weijts,Bart W141Weinhart,Marie M197Weinmüller,Michael T171Weinstein,Lee M215, T185Weiser-Evans,Mary T165Weiss,WilliamA. W081Weissenberger,Jakob M110Weissman,Drew W123Weller,Michael T088Wellner,Gili W174Welsh,Gavin T210Welsh,Michael T105,W024Weng,Linqian W176Weninger,Wolfgang M086,W206Werner,Ann-Cathrin W178Wessel,Florian T201Westermarck,Jukka T088Wettschureck,Nina M004,M075,T106,W170Wevers,N.R. W041Wezel,Anouk M047Wheatcroft,StephenB. M053White,Ian T123Whitehead,Lachlan M092Wickström,Sara T153Wiesner,Cora M031Wietrzyk,Joanna W100Wihuri,Eleonoora T063Wiig,Helge W049Wilczynski,Bartek T024, T196Wilhelm,Kerstin W179Wilkinson,RobertN M016, T188

– 198 –


Wille,Annalena M090, M095Willems,Brecht M146, T002Williams,KevinJon W061Williamson,Gary W151Wilschut,K.J. W041Wilson,Ariel T215,W180Wilting,Jörg W181Winkler,Manuel W182Winter,Birgitta M028Wirth,Angela M075Wirth,Galina M027,T064,W184Wisniewska-Kruk,Joanna T006Wisniewski,Laura W201Wisselink,Willem M043Witasp,Anna M060,W084Wittig,Ilka T084,W094,W109Wittig,Janina M204Woest,Manon W146Wohlfahrt,Thomas W047Wohlfeil,Sebastian T056,T209,W185Wojciak-Stothard,Beata W059,W060Wong,HoYi W013,W014Wong,Vickie M092Wortham,Matthew M033Wu,Bingruo W210Wu,David M133Wu,Junxi W137Wu,Kanxing M076Wu,KennethK. W192Wu,Yingxi M163Xia,Luoxing W129Xin, Mei W187Xiong, Zhen T074Xu, Aimin M073Xu,Ying W208Xu,Youjia W208Yam,Michelle W139Yamamoto,Seiji W188Yan,Yan M156Yang,Chunbo M056Yang,HanMo W189Yang,JeeMyung T098,T199,W190Yang,JiHun M080Yang,Myungjin T044Yang,Pengwei M071Yang,Steven T040Yang,Xiaojuan M200Yang,Youwen M041Yang,Yunlong M200Yaniv,Karina M019, M029, M098, M149, T007,

W134,W136Yard,Benito W103Ye,Zhimin W193Yegutkin,Gennady T116Yeh,Mei-Chun T034Yeo,KimPin W191Yet,Shaw-fang W192Yetkin-Arik,Bahar T052Yeung,KakK. M043

Yim,Evelyn T021Yin,Guonan W195Yin,Xiangke M114,W193,W194Yip,Lisan M219Ylä-Herttuala,Elias W186Ylä-Herttuala,Seppo M020, M027, M113, M175, M193,

M212, M214, T003, T024, T033, T037, T059, T064, T085, T087, T104,T174,T190,T196,W058,W061,W140,W184,W186,W214,W215

Yoder,MervinC. M139Yokokawa,Ryuji T195Yoneyama,Kazuki W197Yoon,Young-sup T094, T095Yosef,Nejla W196Yoshida,Masayuki T211Yoshida,Ryo W127Yoshimatsu,Yasuhiro W197Young,Alison W107Ytterberg,Jimmy M130Yu,Di W175Yu,James T100Yu,Jun W198Yu,Pengchun W199Yu,Ri T041Yu,Wei W200Yu,YoungSuk T011Yudin,Vladimir W032Yudkin,JohnS W152Yuen,TracyJ. W081Yukina,Galina W032Yuldasheva,Nadira M053,W173Z. Adzemovic, Milena T193Zabini,Diana W096Zaborowski,Rafal T024, T196Zachary,Ian W201Zahler, Stefan W034Zakrzewska,Agnieszka M172,W035,W118Zantl, Roman W155Zapotoczny,Bartosz T080Zappe, Maren T062Zarb,Yvette T031Zarkada, Georgia M186Zazerskaya,Irina W101Zeboudj,Lynda T086Zegeye,Mulugeta T219Zeiher, Andreas M. M151Zeisberg,Elisabeth M187Zeitelhofer Adzemovic, Milena

W110,W203

Zeitelhofer, Manuel M141,T193,W110,W203Zeng, Lingfang M056Zeng, Zhi W128,W129Zeni, Filippo M021, T131Zhang, Cheng T027,W198Zhang, Donghong W210Zhang, Ganlin T105Zhang, Hangjun W216Zhang,Huayu M160

– 199 –


Zhang, Lei W200Zhang,Peisheng W108Zhang,Peng W208Zhang,Xinbo M071,W198Zhang,Yan W204Zhang,Yang W205Zhang,Yanyu M064, M181Zhang,Yin M200Zhang,Yuanyuan M209Zhang,Zhenwu W210Zhao, Xiaocheng W207Zhao,Yang M086,W139,W206Zheng,Tuyu W183Zheng, Xiangjian M081Zhou, Bin W200,W210Zhou, Changcheng W211Zhou, Fei W208Zhou,Wenping W209Zhu,Changbin T117Zhu,Weiquan(wendy) W212

Zhuang, Zhen M071Zhuravleva,Kristina W076Zienkiewicz,Aleksandra T022Zierow,Johanna T056,T209,W182,W185Zigmond, Ehud M019Zimmerman, Margaret T109Zinovkina, Nadezhda M168Zuccarini, Mariachiara T116Zuchtriegel,Gabriele W034Zukunft,Sven M205,W112Zwiers,Peter W162,W213Zwijsen,An W158Åhgren, Aive W149Ärnlöv, Johan M064Öffner,Wolfgang W155Örd, Tiit W214,W215Özen, Ilknur W056Öörni, Anssi W061Öörni, Katariina T190,W061

Posters – Monday

– 200 –

IVBM2018

SpeakersSpeakers

Ralf Adams Professor&DirectorMaxPlanckInstituteforMolecular Biomedicine and UniversityofMünsterMünster,Germany

Elisabetta Dejana ProfessorFIRCInstituteofMolecularOncologyandUppsalaUniversityMilan,Italy&Uppsala,Sweden

Anne Eichmann ProfessorYaleSchoolofMedicineNewHaven,CT,USA

Napoleone Ferrara ProfessorUniversityofCaliforniaSan Diego, CA, USA

Holger Gerhardt ProfessorMaxDelbrückCenterforMolecular Medicine Berlin,Germany

Timothy Hla Professor&InvestigatorHarvard Medical School and Boston Children’s HospitalCambridge&Boston,MA,USA

Helen Hobbs Professor&DirectorUTSouthwesternMedicalCenterDallas, TX, USA

Rakesh Jain Professor&DirectorHarvard Medical School andMassachusettsGeneralHospitalCambridgeandBoston,Massachusetts,USA

Mark Kahn ProfessorUniversityofPennsylvaniaPhiladelphia,PA,USA

Gou Young Koh Professor&DirectorKoreaAdvancedInstituteofScienceandTechnologyDaejeon, Korea

Plenary speakers

Posters – Monday

– 201 –

IVBM2018Speakers

Naoki Mochizuki Professor&DirectorNationalCerebralandCardiovascular Center ResearchInstituteOsaka, Japan

Maiken Nedergaard PrincipalInvestigatorUniversityofRochesterMedical CenterRochester,NY,USA

Susan Quaggin Professor&DirectorNorthwesternUniversityChicago, IL, USA

Shahin Rafii ProfessorWeillCornellMedicalCollegeNewYork,NY,USA

William C. Sessa Professor&DirectorYaleSchoolofMedicineNewHaven,CT,USA

Michael Simons ProfessorYaleSchoolofMedicineNewHaven,CT,USA

Didier Stainier Professor&DirectorMaxPlanckInstituteforHeart and Lung ResearchBadNauheim,Germany

Posters – Monday

– 202 –

IVBM2018

Parallel session speakers

ZoltanArany UniversityofPennsylvania Philadelphia,PA,USA

HellmutAugustin UniversityofHeidelberg&GermanCancerResearchCenter Heidelberg,Germany

VictoriaBautch TheUniversityofNorthCarolinaatChapelHill ChapelHill,NC,USA

RuiBenedito CentroNacionaldeInvestigacionesCardiovasculares Madrid,Spain

GabrieleBergers UniversityofLeuven Leuven,Belgium

ChristerBetsholtz KarolinskaInstitutetandUppsalaUniversity Stockholm&Uppsala,Sweden

JoyceBischoff BostonChildren’sHospital Boston,MA,USA

EbbaBrakenhielm RouenandNormandyUniversity Rouen,France

PeterCampochiaro JohnsHopkinsUniversity Baltimore,MD,USA

PeterCarmeliet UniversityofLeuven Leuven,Belgium

MichaelDellinger UTSouthwesternMedicalCenterandTheLymphaticMalformationInstitute

Dallas,TX,USAandBethesda,MD,USA

MicheleDePalma EcolePolytechniqueFédéraledeLausanne Lausanne,Switzerland

MichaelDetmar ETHZürich Zurich,Switzerland

StephanieDimmeler GoetheUniversity FrankfurtamMain,Germany

BrittaEngelhardt UniversityofBern Bern,Germany

UlfEriksson KarolinskaInstitutet Stockholm,Sweden

AndreasFischer GermanCancerCenter Heidelberg,Germany

IngridFleming GoetheUniversity FrankfurtamMain,Germany

GordonFrancis UniversityOfBritishColumbia Vancouver,Canada

BarbaraGarmy-Susini Inserm Toulouse,France

CeciliaGiachelli UniversityofWashington Seattle,WA,USA

MarionaGraupera ProCURE-IDIBELL Barcelona,Spain

JaimeGrutzendler YaleSchoolofMedicine NewHaven,CT,USA

ChenghuaGu HarvardMedicalSchool Cambridge,MA,USA

CorneliaHalin ETHZürich Zurich,Switzerland

NatashaHarvey UniversityofSouthAustralia Adelaide,SA,Australia

YulongHe SoochowUniversity Suzhou,Jiangsu,China

BenHogan UniversityofQueensland Brisbane,QLD,Australia

Young-KwonHong UniversityofSouthernCalifornia LosAngeles,CA,USA

YuHuang ChineseUniversityofHongKong PondCres,MaLiuShui,Hongkong

BeatImhof UniversityofGeneva Geneva,Switzerland

LarsJakobsson KarolinskaInstitutet Stockholm,Sweden

SirpaJalkanen UniversityofTurku Turku,Finland

RandallS.Johnson UniversityofCambridgeandKarolinskaInstitute Cambridge,UK&Stockholm,Sweden

DontschoKerjaschki UniversityofVienna Vienna,Austria

FriedemannKiefer MaxPlanckInstituteforMolecularBiomedicineandUniversityofMünster

Münster,Germany

Hyo-SooKim SeoulNationalUniversityandSeoulNationalUniversityHospital

Seoul,Korea

InjuneKim KoreaAdvancedInstituteofScienceandTechnology Daejeon,Korea

JonathanKipnis UniversityofVirginiaSchoolofMedicine Charlottesville,VA,USA

Speakers

Posters – Monday

– 203 –

IVBM2018

RiikkaKivelä UniversityofHelsinki&WihuriResearchInstitute Helsinki,Finland

YoshiakiKubota KeioUniversitySchoolofMedicine Tokyo,Japan

CalvinKuo StanfordUniversity Stanford,CA,USA

Young-GuenKwon YonseiUniversity Seoul,Korea

FerdinandLeNoble KarlsruheInstituteofTechnology Karlsruhe,Germany

KlausLey LaJollaInstituteforAllergy&Immunology LaJolla,CA,USA

StenLinnarsson KarolinskaInstitutet Stockholm,Sweden

TetsuyaMatoba KyushuUniversityHospital Fukuoka,Japan

DonaldMcDonald UniversityofCaliforniaSanFrancisco SanFrancisco,CA,USA

TaijaMäkinen UppsalaUniversity Uppsala,Sweden

StefanOffermanns MaxPlanckInstituteforHeartandLungResearch BadNauheim,Germany

GooTaegOh EwhaWomansUniversity Seoul,Korea

GuillermoOliver FeinbergCardiovascularResearchInstitute,NorthwesternUniversity

Chicago,IL,USA

GaryOwens UniversityofVirginiaSchoolofMedicine Charlottesville,VA,USA

SamirParikh HarvardMedicalSchool Boston,MA,USA

TatianaPetrova UniversityofLausanneandLudwigInstituteforCancerResearch

Lausanne,Switzerland

KristianPietras LundUniversity Lund,Sweden

MichaelPotente MaxPlanckInstituteforHeartandLungResearch BadNauheim,Germany

AnnaRandi ImperialCollegeLondon&HammersmithHospital London,UK

KristyRed-Horse StanfordUniversity Stanford,CA,USA

YvonneReiss GoetheUniversity FrankfurtamMain,Germany

AnneSaarikko HelsinkiUniversityHospital Helsinki,Finland

PipsaSaharinen UniversityofHelsinki&WihuriResearchInstitute Helsinki,Finland

MikeSapieha UniversityofMontreal Montreal,Canada

StefanSchulte-Merker UniversityofMünster Münster,Germany

MartinA.Schwartz YaleCardiovascularResearchCenter NewHaven,CT,USA

ArndtSiekmann MaxPlanckInstituteforMolecularBiomedicine Münster,Germany

NobuyukiTakakura OsakaUniversity Osaka,Japan

GavinThurston RegeneronPharmceuticals Tarrytown,NY,USA

JaapvanBuul UniversityofAmsterdam Amsterdam,theNetherlands

DietmarVestweber MaxPlanckInstituteofMolecularBiomedicine Münster,Germany

MiikkaVikkula UniversityofLouvain Brussels,Belgium

KennethWalsh UniversityofVirginiaSchoolofMedicine Charlottesville,VA,USA

TetsuroWatabe TokyoMedicalandDentalUniversity Tokyo,Japan

HelgeWiig UniversityofBergen Bergen,Norway

JunK.Yamashita KyotoUniversity Kyoto,Japan

KarinaYaniv WeizmannInstituteofScience Rehovot,Israel

SeppoYlä-Herttuala UniversityofEasternFinland Kuopio,Finland

MasayukiYoshida TokyoMedicalandDentalUniversity Tokyo,Japan

BinZhou ChineseAcademyofSciences Shanghai,China

BerislavZlokovic KeckSchoolofMedicineatUniversityofSouthernCalifornia

LosAngeles,CA,USA

Speakers

Posters – Monday

– 204 –

IVBM2018

Short talks

AndreaBanfi BaselUniversityHospital Basel,Switzerland

AngelaBradshaw UniversityofGlasgow Glasgow,UK

KevinBrulois StanfordUniversity Stanford,CA,USA

LeighCoultas WalterandElizaHallInstituteofMedicalResearch Victoria,Australia

LauriEklund UniversityofOulu Oulu,Finland

YunFang UniversityofChicago Chicago,USA

AlessandroFantin UCLInstituteofOphthalmology London,UK

ClaudioFranco InstitutodeMedicinaMolecular Lisbon,Portugal

JenniferGamble UniversityofSydney Sydney,Australia

EmmaGordon UniversityofQueensland St.Lucia,Australia

ArieHorowitz ThomasJeffersonUniversity Philadelphia,PA,USA

LaurentJacob BrainandSpineInstituteIcm Paris,France

MichaelJeltsch UniversityofHelsinki Helsinki,Finland

Suk-wonJin GwangjuInstituteofScienceandTechnology NewHaven,CT,USA

ElizabethJones KuLeuven Leuven,Belgium

MinnaKaikkonen-Määttä UniversityofEasternFinland Kuopio,Finland

RaghuKataru MemorialSloanKetteringCancerCenter NewYork,NY,USA

Bong-IhnKoh KoreaAdvancedInstituteofScienceandTechnology Daejeon,Korea

PeppiKoivunen UniversityofOulu Oulu,Finland

ThomasKorff HeidelbergUniversity Heidelberg,Germany

MurielLaffarque InsermUmr1048 Toulouse,France

XuriLi SunYat-SenUniversityinGuangzhou Guangzhou,China

AmandaLund OregonHealth&ScienceUniversity Portland,OR,USA

IlseLuyckx UniversityOfAntwerp Antwerpen,Belgium

MasatakaMajima KitasatoUniversitySchoolofMedicine Kanagawa,Japan

StephenMoss UCLInstituteofOphthalmology London,UK

SarahMueller DukeUniversity Durham,NC,USA

WilliamA.Muller NorthwesternUniversityFeinbergSchoolOfMedicine Chicago,IL,USA

DebabrataMukhopadhyay MayoClinicCollegeOfMedicineAndScience Jacksonville,FL,USA

OsamuNakagawa NationalCerebralandCardiovascularCenter Osaka,Japan

StefaniaNicoli YaleCardiovascularResearchCenter NewHaven,CT,USA

AgnèsNoel UniversityofLiege Liège,Belgium

TimothyPadera HarvardMedicalSchool Cambridge,MA,USA

MiaPhillipson UppsalaUniversity Uppsala,Sweden

ChristianRamakers Mimetas Leiden,TheNetherlands

MarkRichards UppsalaUniversitet Uppsala,Sweden

GiorgioSeano InstitutCurieResearchCenter Paris,France

MahakSinghal GermanCancerResearchCenter Heidelberg,Germany

RaduV.Stan GeiselSchoolofMedicineatDartmouth Hanover,NH,USA

AkiraTakeda UniversityOfTurku Turku,Finland

PatricTurowski UniversityCollegeLondon London,UK

BernardM.vandenBerg LeidenUniversityMedicalCenter Leiden,theNetherlands

MichaelVanlandewijck UppsalaUniversitet Uppsala,Sweden

Anne-ClemenceVion UniversityofNantes Nantes,France

MeiXin CincinnatiChildren’sHospital Cincinnati,OH,USA

Speakers

Posters – Monday

– 205 –

IVBM2018

KimPinYeo NationalUniversityOfSingapore Singapore,Singapore

QiZhao Regeneron Tarrytown,NY,USA

Speakers

Posters – Monday

– 206 –

IVBM2018

Einari Aavik, UniversityofEasternFinlandAbdallahAbuTaha, UppsalaUniversityMarcAchen, PeterMaccalllumCancerCentreRalfAdams, MPIforMolecularBiomedicineWillAdams, RiparianPharmaceuticalsMonaAhmed, KarolinskaInstitutetKatjaAhokas, PromegaBiotechAbAlexanderAinscough, ImperialCollegeLondonKittiAjtay, SemmelweisUniversityLuisAlarconMartinez, UniversityofMontrealJulianAlbarranJuarez, MPIforHeart&LungResearchYvonneAlexander,ManchesterMetUniversityNicoletaAlexandru, InstCellBio&PathKariAlitalo, UniversityofHelsinki&WRIJenniferAllport-Anderson,NovartisInstitutesReginaldoAlmeidadaTrindade,UniversityMedicalCenterGRFlorianAlonso, UniversityofBordeauxAlbertoAlvarez-Aznar, UppsalaUniversitySanniAlve, UniversityofHelsinkiGustavoAlviter-Raymundo,MPIforMolecularBiomedicineMinnaAmpuja, UniversityofHelsinkiKarthikAmudhalaHemanthakumar, WRI&UniveristyofHelsinkiMaarjaAndaloussiMäe, UppsalaUniversityKoji Ando,UppsalaUniversityJohanna Andrae,UppsalaUniversityLaetitia Andrique,InsermU1029Andrey Anisimov,WRI&UniveristyofHelsinkiSalli Antila,WRI&UniveristyofHelsinkiZolt Arany,UniversityofPennsylvaniaNida Arif,MPIforMolecularBiomedicineAngel Armesilla,UniversityofWolverhamptonEmma Armstrong,WihuriResearchInstituteCaroline Arnold,HeidelbergUniversityMarkChristopher Arokiaraj,PondicherryInstituteAmita Arora,MinervaFoundationGonzalo ArtiachCastanon,KarolinskaInstitutetLihee Asaf,WeizmannInstituteNursabah, Atli,UniversityofEastAngliaHellmut, Augustin,HeidelbergUniversityMohan, Babu,UniversityofEasternFinlandMagnus, Back,KarolinskaUniversityHospitalJungHyun, Bae,IBSSunSik Bae,PusanNationalUniversityFabiana Baganha,LeidenUniversityMedicalCenterSabine Bailly,InsermAndrew Baker,UniversityofEdinburghErik Bakker,AmcLászló Bálint,SemmelweisUniversityAndrea Banfi,BaselUniversityHospitalUlrike Baranyi,MedicalUniversityofViennaIvan Bassi,WeizmannInstituteVictoria Bautch,UniversityofNorthCarolinaSandra Beeske,SanofiHeinz-Georg Belting,Biozentrum/UniversityofBaselOrina Belton,UniversityCollegeDublinHugh Bender,UniversityofCaliforniaIrvineRui Benedito,CNICGabriele Bergers,VIB-CenterforCancerBiologyMustafaBeter,UniversityofEasternFinlandChrister Betsholtz,UppsalaUniversityAndreas Beyer,MedicalCollegeofWisconsinAparna Bhattacharyya,DrexelUniversityColette Bichsel,BostonChildren’sHospitalErk Biessen,MaastrichtUniversity

ParticipantsParticipants

Andreas Bikfalvi,InsermU1029Diewertje Bink,VUMedicalCenterAmsterdamGraeme Birdsey,ImperialCollegeLondonJoyce Bischoff,BostonChildren’sHospitalGiulia Boezio,MPIforHeart&LungResearchNatalijaBogunovic,VUMedicalCenterAmsterdamMarie-LuceBochaton-Piallat,UniversityofGenevaIsabelle Boitel-Barbosa,SanofiRebecca Bolton,UclClaudine Bonder,CentreforCancerBiologyElisa Boscolo,CincinnatiChildren’sHospitalIlze Bot,LACDR/LeidenUniversityGwenola Boulday,InsermAngela Bradshaw,UniversityofGlasgowEbba Brakenhielm,InsermKarim Brandt,UniversityofGenevaLaura Braun,MPIforMolecularBiomedicineNathalie Brouard,Efs-insermKevin Brulois,StanfordUniversitySarah Bruneau,InstermUMR1064Alexander-FranciscoBruns,UniversityofLeedsLynn Butler,KarolinskaInstitutetKristina ByskovUniversityofOsloRachel, CainesQueen’sUniversityBelfastPeter CampochiaroWilmerOpthalmologicalInstituteAnnaRita, CantelmoVIB-KULeuvenJiahui Cao,UniversityofMünsterAndrea Caporali,UniversityofEdinburghLuísMiguelCardosoDosSantos,CMU-UNIGEClaudia Carlantoni,MPIforHeart&LungResearchPeterCarmeliet,KULeuven-VIBCenterMiguel CarracedoOrtiz,KarolinskaInstitutetSian Cartland,HeartResearchInstituteMarco Castro,UppsalaUniversityJessica Cedervall,UppsalaUniversityYinTungCrystal Chan,UniversityofHongKongJeanne Chang,CellBiologics,Inc.Candice Chapouly,InsermU1034Brahim Chaqour,SunyDownstateMedicalCenterLee-Young Chau,AcademiaSinicaHong Chen,HarvardMedicalSchoolRongyuan Chen,SunYat-senUniversityShuo Chen,UniversityofHelsinkiXinyi Chen,UniversityofHongKongPei-Yu Chen,YaleUniversityRamesh Chennupati,MPIforHeart&LungResearchChristineCheung,NanyangTechnologicalUnivSamantha Chew,NationalUniversityofSingaporeAyano Chiba,NatlCerebr&CardiovascCenterHavovi Chichger,AngliaRuskinUniversityAnilKumarChikkasiddeGowda,ZhongshanOphthalmicCenterDmitri Chilov,UniversityofHelsinkiSudhakarChintharlapalli,EliLilly&Company Stefan Chlopicki,JagiellonianUniversityYoungkyu Cho,KoreaUniversitySeungbum Choi,GachonResearchInstituteJeongwoon Choi,IBSSeung-Cheol Choi,KoreaUniversityJaesungPeter Choi,UniversityofSydneyMan Chu,CyrusTangHematologyCenterJuhye Chung,CatholicUniversityofKoreaGiorgia Ciliberti,GoetheUniversityFrankfurtLena Claesson-Welsh,UppsalaUniversityPaul Coleman,CentenaryInstitute

Posters – Monday

– 207 –

IVBM2018Participants

Kerrie Collins,UniversityofIllinoisatChicagoAlinaConstantin,InstCellBio&PathLei Conze,UppsalaUniversityIsabelle Coornaert,UniversityofAntwerpMonica Corada,Ifom-FircJuliette Coudert,IpbsLeigh Coultas,Walter&ElizaHallInstituteBaptiste Coxam,MDCforMolecularMedicineHenar Cuervo,UniversityofIllinoisatChicagoSaraCunha,UppsalaUniversitySilke Currie,MPIforMolecularBiomedicineRosalia D’Angelo,UniversityofMessinaKatrine DahlBjørnholm,UniversityofCopenhagenRudra Das,WeizmannInstituteofScienceNina Daubel,UppsalaUniversityThomas Daubon,InsermU1029Sascha David,MedicalSchoolHannoverKatrien DeBock,ETHZürichEster delaCruz,CNICJo DeMey,UniversityofSouthernDenmarkGuido DeMeyer,UniversityofAntwerpDorien DeMunck,UniversityofAntwerpMichele DePalma,EPFLCarlie DeVries,AcademicMedicalCenterAMSMargreet DeVries,LeidenUniversityMedicalCenterElga DeVries,VuMedicalCenterVivian DeWaard,AcademicMedicalCenterAMSElisabeth Deindl,Walter-Brendel-CentreElisabetta Dejana,Ifom-Firc&UppsalaUniversityNicole Dekker,VUMedicalCenterAmsterdamMichael Dellinger,UTSouthwesternMedicalCenterJasper Demandt,MaastrichtUniversityAgnes Desroches-Castan,InsermMichael Detmar,EthZurichMatthew Detter,DukeUniversityPratibha Dhumale,UniversityofSouthernDenmarkHiramani Dhungana,UniversityofEasternFinlandMannekombaDiagbouga,UniversityofGenevaMariangela DiTacchio,EdingerInstituteAnna Dimberg,UppsalaUniversityStefanie Dimmeler,GoetheUniversityFrankfurtMonkamDjopgangEpseNzeuhangChristelle,AtlanticMedicalCentreAlison Domingues,Umrs1140IThEMNicholas Downes,UniversityofEasternFinlandYuxiang Du,SunYat-senUniversityAlexandre Dubrac,YaleUniversityPascale Dufourcq,InsermU1034Neil Dufton,ImperialCollegeLondonJozef Dulak,JagiellonianUniversityKevin Dunn,PromocellGmbhCaoNguyen Duong,MPIforMolecularBiomedicinePhilip Dusart,ScilifelabJochen Dutzmann,HannoverMedicalSchoolLowell Edgar,UniversityofEdinburghDominik Eichin,UniversityofTurkuAnne Eichmann,YaleUniversityLauri Eklund,UniversityofOuluSammy El-Mansi,UniversityofGlasgowFanny Elahi,UniversityofCaliforniaSFHarri Elamaa,UniversityofOuluKyrre Emblem,OsloUniversityHospitalBritta Engelhardt,UniversityofBernBernadette Englert,NAVBOUlf Eriksson,KarolinskaInstitutetEtto Eringa,VUMedicalCenterAmsterdamCharlotte Erpicum,BostonChildren’sHospital

Maria-FrancescaEvaristi,SanofiBernah Fahning,UniversityofSãoPauloRuth Fair-Mäkelä,UniversityofTurkuDinara FaizullinaStPetersburgMedicalUniversityAnnelie Falkevall,KarolinskaInstitutetYun Fang,UniversityofChicagoShentong Fang,WihuriResearchInstituteAlessandro Fantin,UniversityCollegeLondonNavid Farahani,3scanEva Faurobert,CnrsUmr5309Laura Fellman,WihuriResearchInstituteAndreia Fernandes,ETHZurichNapoleone Ferrara,UniversityofCaliforniaSDMaria Filippova,BaselUniversityHospitalPauliina Filppu,UniversityofHelsinkiAndreas Fischer,GermanCancerResearchCenterStephen Fitzsimons,UniversityCollegeDublinIngrid Fleming,GoetheUniversityErika Folestad,KarolinskaInstitutetMiriamHelenaFonseca-Alaniz,UniversityOfSãoPauloRudolf Fontijn,VUMedicalCenterAmsterdamSylvain Fraineau,InsermU1096Gordon Francis,UniversityofBritishColumbiaClaudio Franco,InstitutodeMedicinaMolecularLinda Fredriksson,KarolinskaInstitutetMaike Frye,UppsalaUniversityMisato Fujita,KanagawaUniversityShigetomo Fukuhara,NipponMedicalSchoolMoe Fukumoto,NatlCerebr&CardiovascCenterGosia Furmanik,MaastrichtUniversityKnut Fälker,ÖrebroUniversityAlishaGM,UniversityofHelsinkiKonstantin Gaengel,UppsalaUniversityCarl Gahmberg,UniversityofHelsinkiJennifer Gamble,CentenaryInstituteAna-Maria Gan,NenckiInstituteDana Gancz,WeizmannInstituteofScienceKeerthana Ganesh,UniversityofHelsinkiMaria GarciaCollado,UppsalaUniversityMarina GarciaGarrido,F.Hoffmann-laRocheLtd.BarbaraGarmy-Susini,InsermAikaterini Gatsiou,GoetheUniversityFrankfurtSébastien Gauvrit,MPIforHeart&LungResearchAnnaGdula,MedicalUniversityofLodzYun Ge,KyungpookNationalUniversityVéronique Gebala,SpringerNatureElisabeth Genot,InsermMaria Georganaki,UppsalaUniversityMaria Georgiadou,UniversityofTurkuHolger Gerhardt,MDCforMolecularMedicineStéphane Germain,INSERMU1050Rebekka Gerschütz,MPIforMolecularBiomedicineIlse Geudens,VIB-KULeuvenCecilia Giachelli,UniversityofWashingtonRoberto GianniBarrera,BaselUniversityHospitalMonica Giannotta,Ifom-FircRainer Glass,LudwigMaximiliansUniversityAlexandre Glemain,Itun-crtiInsermUmr1064Maria Globisch,UppsalaUniversityEllen Go,IndianaUniversityAlejandro Godoy,CatholicUniversityofChileDelphine Gomez,UniversityofPittsburghJesus GomezEscudero,QueenMaryUniversityEmma Gordon,UniversityofQueenslandLeonor Gouveia,UppsalaUniversitySilvia Gramolelli,UniversityofHelsinkiMariona Graupera,Idibell

Posters – Monday

– 208 –


John Greenwood,UniversityCollegeLondonRandy Grimlowski,MPIforMolecularBiomedicineAnna Grochot-Przeczek,JagiellonianUniversityJaime Grutzendler,YaleUniversityMikaela Grönholm,UniversityofHelsinkiChenghua Gu,HarvardMedicalSchoolAdrie Gubbels,FujifilmVisualsonicsErika Gucciardo,UniversityofHelsinkiJasenka Guduric-Fuchs,Queen’sUniversityBelfastHind Guenou,InsermU1197Erika Gurzeler-Tiihonen,UniversityofEasternFinlandGuillaume Ha,InsermU1197JungMin Ha,PusanNationalUniversityJean Habyarimana,JanvierLabsPaul Hacking,ManninResearchRene Haegerling,StGeorge’sUniversityLaura Hakanpää,UniversityofHelsinkiCornelia Halin,EthZurichAnahita Hamidi,UppsalaUniversityJung-Hwa Han,YeungnamUniversityToshiro Hara,FukuokaChildren’sHospitalCharlotteHarkenJensen,OdenseUniversityHospitalMartin Harmsen,UniversityMedicalCenterGRAdrian Harris,UniversityofOxfordNatasha Harvey,UniversityofSouthAustraliaYulong He,SoochowUniversityLiqun He,TianjinMedicalUniversityUlf Hedin,KarolinskaInstitutetMarie Hedlund,UppsalaUniversityHanna Heikkilä,UniversityofHelsinkiIrina Hein,ibidiGmbHKrista Heinolainen,WihuriResearchInstituteEmmi Helle,UniversityofHelsinkiDominique Helley,HôpitauxdeParisAlexandra Helmke,MedicalSchoolHannoverEmeli Hermansson,UppsalaUniversityCarlos Hermenegildo,UniversityofValenciaMagda Hernandez,UppsalaUniversityMelanie Herre,UppsalaUniversityKyoko Hida,HokkaidoUniversityYasuhiro Hida,HokkaidoUniversityHannah Hills,CaltagMedsystemsPatricia Himmels,GenentechInc.Karen Hirschi,YaleUniversityYu Hisano,BostonChildren’sHospitalTimothy Hla,BostonChildrensHospitalTerri Hnatyszyn,3scanHelen Hobbs,UTSouthwesternMedicalCenterBen Hogan,UniversityofQueenslandKrista Hokkanen,UniversityofEasternFinlandMaija Hollmén,UniversityofTurkuWolfgang Holnthoner,Ludwig-Boltzmann-InstitituteHyunSook Hong,KyungHeeUniversityYoung-Kwon Hong,UniversityofSouthernCaliforniaNaoki Honkura,UppsalaUniversityEsther Hoppe,MPIforMolecularBiomedicineAnke Hoppensack,FreieUniversitaetBerlinPeter Hordijk,VUMedicalCenterAmsterdamArie Horowitz,ThomasJeffersonUniversityAnton Horrevoets,VUMedicalCenterAmsterdamKayoko Hosaka,KarolinskaInstitutetAlfons Houben,MaastrichtUMC+László Hricisák,SemmelweisUniversityJiong Hu,GoetheUniversityYichao Hua,VIBYu Huang,ChineseUniversityofHongKongChristopherHughes,UCIrvine

Elisabeth Huijbers,VUMedicalCenterNan Hultgren,UniversityofCaliforniaIrvineEvelyn Hutterer,KarolinskaInstitutetHenri Huttunen,HerantisPharmaPlcByungtae Hwang,KoreaResearchInstituteSharon Hyduk,UniversityHealthNetworkOlli-Pekka Hätinen,UniversityofEasternFinlandTomohiro Iba,OsakaUniversityHenna Ilmonen,UniversityofEasternFinlandBeat Imhof,UniversityofGenevaGulayse InceDunn,UniversityofHelsinkiDonato Inverso,GermanCancerResearchCenterAndras Iring,MPIforHeart&LungResearchLuisaIruela-Arispe,UCLAGriselda Irusta,IBYMETomohiko Ishibashi,NatlCerebr&CardiovascCenterYoshinori Ito,SendaiAerClinicFumiko Itoh,TokyoUniversityVikram Iyer,UniversityofQueenslandSarah Jackson,JournalofClinicalInvestigationDavid Jackson,UniversityofOxfordLaurent Jacob,Brain&SpineInstitueICMSousan Jafari,UniversityofOuluRakesh Jain,HarvardMedicalSchoolLars Jakobsson,KarolinskaInstitutetZoltánPéter Jakus,SemmelweisUniversitySirpa Jalkanen,UniversityofTurkuArmand Jaminon,MaastrichtUniversityHyunduk Jang,SeoulNationalUniversityThomas Janvier,JanvierLabsJozsef Jaszai,TUDresdenMatti Jauhiainen,MinervaFoundationSuvi Jauhiainen,UppsalaUniversityMarie Jeansson,UppsalaUniversityMichael Jeltsch,UniversityofHelsinkiScott Jenkins,3ScanNina Jensen,KarolinskaInstitutetJae-Hoon Jeong,KoreaInstituteJunHa Jeong,KyungHeeUniversityAyelet Jerafi-Vider,WeizmannInstituteofScienceSawanKumar Jha,UniversityofHelsinkiSuk-Won Jin,GwangjuInstituteShaobo Jin,Icmc,KarolinskaInstitutetYi Jin,UppsalaUniversityDongHyun Jo,SeoulNationalUniversityYoungAe Joe,CatholicUniversityofKoreaRandall Johnson,UniversityofCambridge&KIElizabeth Jones,KULeuvenRianne Jongman,UMCGCamille Jost,Efs-insermHyojee Joung,SeoulNationalUniversityAri Jouppila,Bio-radLaboratoriesAnnukka Jouppila,HUCHResearchInstituteAurélie Joussaume,InsermU1082Eva JoverGarcia,UniversityofBristolRong Ju,SunYat-senUniversityJihyun Jung,KyungHeeUniversityRio Juni,VUMedicalCenterAmsterdamPatrick Jurney,OregonHealth&ScienceUnivHannu Järveläinen,UniversityofTurkuTero Järvinen,UniversityofTampereKatarina Jääskeläinen,HerantisPharmaPlcJun Ka,GISTMika Kaakinen,UniversityofOuluNeliKachamakova-Trojanowska,JagiellonianUniversityMark Kahn,UniversityofPennsylvaniaMinnaKaikkonen-Määttä,UniversityofEasternFinland

Posters – Monday

– 209 –


Susanna Kaisto,UniversityofOuluMikko Kajovaara,Bio-RadLaboratoriesABPauliina Kallio,UniversityofHelsinkiSeok Kang,IBSMeikeHedwigKeuters,UniversityofEasternFinlandLi Kang,KyungpookNationalUniversityEmmi Kapiainen,UniversityofOuluSinem Karaman,WRI&UniveristyofHelsinkiChristina Karapouliou,StGeorge’sUniversityHelena Karlström,KarolinskaInstitutetRaghu Kataru,MSKCCPritinder Kaur,CurtinUniversityAndrius Kazlauskas,UniversityofIllinoisatChicagoAnnikaKeller,UniversityHospitalZürichMolly Kelly-Goss,UniversityofVirginiaAapeli Kemppainen,WihuriResearchInstituteDontscho Kerjaschki,MedicalUniversityofViennaEli Keshet,HebrewUniversitySanna Kettunen,UniversityofEasternFinlandLevon Khachigian,UniversityofNewSouthWalesIvanaKholova,UniversityofTampereHiroyasu Kidoya,OsakaUniversityFriedemann Kiefer,WWUMünsterMiika Kiema,UniversityofEasternFinlandMinna Kihlström,UniversityofOuluSehong Kim,CatholicUniversityofKoreaHyung-Seok Kim,ChonnamNationalUniversityJaetaek Kim,Chung-AngUniversitySeoKi Kim,IBSKyunHoo Kim,InstituteforBasicScienceInjune Kim,KAISTPilhan Kim,KAISTSooHyun Kim,KAISTDo-Geun Kim,KoreaBrainResearchInstituteMirim Kim,KoreaUniversityJaeHo Kim,PusanNationalUniversityHyo-Soo Kim,SeoulNationalUniversityMinah Kim,UniversityofCaliforniaSFBoa Kim,UniversityofPennsylvaniaSeulGi Kim,YeungnamUniversitySuji Kim,YeungnamUniversitySujin Kim,YeungnamUniversityDongYoung Kim,YonseiUniversityJoori Kim-Kaneyama,ShowaUniversityJonathan Kipnis,UniversityofVirginiaElina Kiss,UniversityofHelsinkiJan Kitajewski,UniversityofIllinoisatChicagoRiikkaKivelä,UniversityofHelsinki&WRIVesa Kiviniemi,OuluUniversityHospitalIngeborg Klaassen,AcademicMedicalCenterJan Klohs,UniversityofZurichPetra Knaus,FreieUniversitaetBerlinKai Knöpp,HannoverMedicalSchoolJihoon Ko,SeoulNationalUniversityPhilipp-Sebastian Koch,HeidelbergUniversityGouYoung Koh,InstituteforBasicScience/KAISTBong-IhnKoh,KAISTPeppi Koivunen,UniversityofOuluEmmi Kokki,UniversityofEasternFinlandKaska Koltowska,UppsalaUniversityChristopher Kontos,DukeUniversityAnnika Koponen,MinervaFoundationThomas Korff,HeidelbergUniversityEmilia Korhonen,WihuriResearchInstitutePetra Korpisalo-Pirinen,UniversityofEasternFinlandRuth-Maria Korth,Fida

Aleksandra Kostina,AlmazovResearchCentreIgor Kovacevic,VUMedicalCenterAmsterdamTom Kovala,NorthernOntarioSchoolofMedPetriKovanen,WihuriResearchInstituteCamille Kowalski,GenevaMedicalSchoolVeerle Kremer, AmcGuido Krenning,UniversityMedicalCenterGRLarissa Kruse,UniversityOfAppliedSciencesYoshiaki Kubota,KeioUniversityTimara Kuiper,UniversityMedicalCenterGRChiaHuang Kuo,BuddhistTzuChiHospitalCheng-Chin Kuo,NatHealthResearchInstitutesCalvin Kuo,StanfordUniversitySuvi Kuosmanen,UniversityofEasternFinlandKondaBabuKurakula,LeidenUniversityMedicalCenterEwa Kurzejamska,LundUniversityEdyta Kus,JagiellonianUniversityBrenda Kwak,UniversityofGenevaDuk-Hwa Kwon,ChonnamNationalUniversityYoo-Wook Kwon,SeoulNationalUniversityYoungGuen Kwon,YonseiUniversitySteffenEmil Künzel,YaleUniversityKristiina Kyrklund,HelsinkiChildren’sHospitalSinaWietje Kürschner,HeidelbergUniversityAnastasia Kyselova,InstituteforVascularSignallingJohanna Laakkonen,UniversityofEasternFinlandPirjo Laakkonen,UniversityofHelsinkiPatrick Lacolley,InsermU1116Muriel Laffargue,InsermNihay LahamKaram,UniversityofEasternFinlandOuti Lahdenperä,HerantisPharmaPlcPäivi Lakkisto,UniversityofHelsinkiVadim LeJoncour,UniversityofHelsinkiFerdinand LeNoble,KarlsruheInstituteofTechnologyFranck Lebrin,LUMCEunhyeong Lee,KAISTJingu Lee,KAISTJaeyeon Lee,KoreaUniversityHyeSun Lee,PusanNationalUniversityByungjun Lee,SeoulNationalUniversitySeokJae Lee,SeoulNationalUniversityEujin Lee,UniversityofTokyoWoo Je Lee,UniversityofUlsanMonica Lee,YaleUniversityShin-Jeong Lee,YonseiUniversityKaisa Lehti,UniversityofHelsinkiSatu Lehti,WihuriResearchInstituteHeli Lehtonen,PfizerOyVeli-Matti Leppänen,WihuriResearchInstituteShulamit Levenberg,IsraelInstituteofTechnologyAnna-Liisa Levonen,UniversityofEasternFinlandKlaus Ley,LaJollaInstituteRui Li,MPIforHeart&LungResearchTomYu-TungLi,MPIforMolecularBiomedicineTaotao Li,SoochowUniversityXiujuan Li,SoochowUniversityXuri Li,SunYat-senUniversityZhilin Li,UniversityofHelsinkiEduardoLinckMachadoGuimaraes,KarolinskaInstitutetSarah Lindsey,TulaneUniversityRenjing Liu,CentenaryInstituteDong Liu,MorehouseSchoolofMedicineXiaolei Liu,NorthwesternUniversityOscar Liu,UniversityofEasternFinlandCecília LlaóCid,UniversityofFrankfurtFrancesco LoPresti,SanofiResearch

Posters – Monday

– 210 –


Tatiana Lobo,WeillCornellMedicineQatarAgnieszka Loboda,JagiellonianUniversityBart Loeys,UniversityOfAntwerpFanny Loisel,InsermU1197Karolina Losenkova,UniversityofTurkuSirpa Loukovaara,HelsinkiUniversityHospitalLaura LouzaoMartinez,UMCUtrechtDominic Love,UppsalaUniversityNoelia Lozano-Vidal,VUMedicalCenterAmsterdamRoberta Lugano,UppsalaUniversityAmanda Lund,OHSUJian Luo,PaloAltoVeteransInstituteIlse Luyckx,UniversityOfAntwerpRuth Lyck,UniversityOfBernQing Ma,UTMDAndersonCancerCenterBriaMacklin,JohnsHopkinsUniversityClaudio Maderna,Ifom-FircSudarrshan Madhavan,UniversityOfHelsinkiYong-Sun Maeng,YonseiUniversityJohanna Magga,UniversityofOuluPeetra Magnusson,UppsalaUniversityMasataka Majima,KitasatoUniversityJisca Majolee,VUMedicalCenterAmsterdamAnna Malashicheva,AlmazovResearchCentreTsveta Malinova,AcademicMedicalCenterAMSMatteo Malinverno,Ifom-FircHadjer Mamoune,InsermU1148LvtsLuigi Mancinelli,CentroCardiologicoMonzinoXue Manz,VUMedicalCenterAmsterdamBrian Mao,UniversityofIllinoisatChicagoMarionMarchand,INSERMU1050Laura Martin,BioscientificaWim Martinet,UniversityofAntwerpInes Martinez-Corral,UppsalaUniversityThomas Mathivet,Parcc-Hegp-InsermU970Ljubica Matic,KarolinskaInstitutetTetsuya Matoba,KyushuUniversityKen Matsumoto,VibYukiko Matsunaga,UniversityofTokyoMaximilian Matthies,UniversityofSouthernDenmarkVirginie Mattot,CNRS-UMR8161Laetitia Mauge,InsermU970ParccGaëlle Mawambo,UniversityOfMontrealUlrike May,UniversityofTampereSandra Mayr,UniversityOfAppliedSciencesTimothy McCord,DukeUniversityJessica McCormack,UniversityCollegeLondonDonald McDonald,UCSFReinhold Medina,Queen’sUniversityBelfastAnnika Mehlem,KarolinskaInstitutetHarry Mellor,UniversityofBristolJohn Mercer,UniversityofGlasgowNathalie Mercier,INSERMU1116Nasrin Mesaeli,WeillCornellMedicineQatarPetra Miikkulainen,UniversityofTurkuClint Miller,UniversityofVirginiaJeong-Ki Min,KoreaResearchInstituteGyongjuElizabeth Min,YaleUniversityAlexandre Mironov,Ifom-FircYekaterina Miroshnikova,HiLIFE&WRIAyumi Miyakawa,UniversityOfSaoPauloTakuro Miyazaki,ShowaUniversityNaoki Mochizuki,NatlCerebr&CardiovascCenterGrietje Molema,UniversityMedicalCenterGREloi MontanezMiralles,LudwigMaximiliansUniversityCorey Monteith,3scan

Hector Monzo,UniversityofHelsinkiJieun Moon,KAISTCarolina MoraesCabe,InstitutCochin-InsermU1016Manuel Morales-Ruiz,HospitalClínic-idibapsPierre Moreau,UniversityofEasternFinlandSandrine Morel,UniversityofGenevaFlorent Morfoisse,UniversityofLiege-GIGACenterEricMorin,UppsalaUniversityJunji Moriya,PmdaNanami Morooka,OsakaUniversitySofia Morsing,SanquinMathilde Mosca,JanvierLabsJill Moser,UniversityMedicalCenterGRNoga Moshe,WeizmannInstituteofScienceStephen Moss,UclInstituteofOphthalmologyKaren Moulton,UniversityofColoradoOlga Mucha,JagiellonianUniversitySarah Mueller,DukeUniversityLars Muhl,KarolinskaInstitutetDev Mukhopadhyay,MayoClinicWilliam Muller,NorthwesternUniversityJoseManuelMunozFelix,QueenMaryUniversityFumitaka Muramatsu,OsakaUniversityTakahisa Murata,UniversityofTokyoIsidore Mushimiyimana,UniversityofEasternFinlandTenderano Muzorewa,DrexelUniversitySeverin Mühleder,LudwigBoltzmannInstituteTaija Mäkinen,UppsalaUniversitySophie Nadaud,Umrs1166Taliha Nadeem,UniversityofIllinoisatChicagoKhayrunNahar,UppsalaUniversityL.A. Naiche,UniversityofIllinoisatChicagoHisamichiNaito,OsakaUniversityHironori Nakagami,OsakaUniversityOsamu Nakagawa,NatlCerebr&CardiovascCenterHiroyuki Nakajima,NatlCerebr&CardiovascCenterYoshikazu Nakaoka,NatlCerebr&CardiovascCenterHironao Nakayama,HiroshimaIntUniversityAkiko Nakayama,MPIforHeart&LungResearchElisabethNaschberger,UK-ErlangenAlice Neal,UniversityofOxfordMaiken Nedergaard,UniversityofCopenhagenAlexandra Newman,UniversityofVirginiaSu Nguyen,WihuriResearchInstituteStefania Nicoli,YaleUniversityEssi Niemi,OsloUniversityHospitalIngrid Nilsson,KarolinskaInstitutetTakeshi Ninchoji,UppsalaUniversityFrankChenfei Ning,KarolinskaInstitutetKoichi Nishiyama,KumamotoUniversityHenri Niskanen,UniversityofEasternFinlandAnja Nitzsche,InsermU970Valerie Nivet-Antoine,UmrS1140Agnes Noel,UniversityofLiegeTaeWook Noh,KAISTJi-Min Noh,KoreaUniversityMarthe NorreenThorsen,K.G.JebsenTRECAstrid Nottebaum,MPIforMolecularBiomedicineSusana Novella,UniversityofValenciaHarri Nurmi,WRI&UniveristyofHelsinkiDaniel Nyqvist,KarolinskaInstitutetStefan Offermanns,MPIforHeart&LungResearchGooTaegOh,EwhaWomansUniversityWon-Jong Oh,KoreaBrainResearchInstitutePäivi Ojala,UniversityofHelsinkiYoshiaki Okada,OsakaUniversity

Posters – Monday

– 211 –


Roxana Ola,YaleUniversityJoppe Oldenburg,UppsalaUniversityDaniel Oliveira,KarolinskaInstitutetMarta Oliveira,MaxDelbrückCenterGuillermo Oliver,NorthwesternUniversityVesa Olkkonen,MinervaFoundationVictor Olsavszky,HeidelbergUniversityAnna-Karin Olsson,UppsalaUniversityKaren Onions,UniversityofBristolMizuko Osaka,TokyoMedical&DentalUnivTomohiro Osanai,HirosakiUniversityNoriko Oshima,TokyoMedical&DentalUnivGeorge Osol,UniversityofVermontVivianne Otto,ETHZurichMalika Oubaha,MontrealUniversityClara Oudenaarden,LundUniversityGary Owens,UniversityofVirginiaIlkka Paatero,UniversityofTurkuJere Paavola,MinervaFoundationTimo Paavonen,UniversityofTampereSara Paccosi,UniversityofFlorenceTimothy Padera,MassachusettsGeneralHospitalJennifer Paech,WihuriResearchInstituteJingxuan Pan,SunYat-senUniversityFernanda Parborell,IBYMEAstrid Parenti,UniversityofFlorenceSamir Parikh,HarvardMedicalSchoolChanSeok Park,CatholicUniversityofKoreaKyu-Hwan Park,DaeguVeteransHospitalIntae Park,IBS/KAISTMi-Jung Park,InjeUniversityChanSoon Park,KAISTJong-Gil Park,KoreaResearchInstituteYongdoo Park,KoreauniversityJaeHyoung Park,KoreaUniversityAnamHospitalHyeRim Park,KyungHeeUniversityKyungWoo Park,SeoulNationalUniversityCheol-Young Park,SungkyunkwanUniversityJoongYeol Park,UniversityofUlsanJeongAe Park,YonseiUniversityNatalia Pascuali,IBYMEJatin Patel,UniversityofQueenslandFrancesca Patella,UniversityCollegeLondonGesine Paul,LundUniversityMichele Paulo,UniversityofSãoPauloClaire Peghaire,ImperialCollegeLondonElisa Peixoto,Queen’sUniversityBelfastToini Pemmari,UniversityofTampereTor PerssonSkare,UppsalaUniversityKevin Peters,AerpioTherapeuticsMilena Petkova,UppsalaUniversityTatiana Petrova,UniversityofLausannePhat Pham,VuMedicalCenterMia Phillipson,UppsalaUniversityJiyuan PiaoKyungHeeUniversityIlkka Pietilä,UppsalaUniversityRiikka Pietilä,UppsalaUniversityKristian Pietras,LundUniversityAnne Pink,UniversityofHelsinkiEdward Plow,ClevelandClinicPaulina Podkalicka,JagiellonianUniversityBruno Poirier,SanofiDawid Polak,MedicalUniversityofLodzChanele Polenz,UniversityHealthNetworkThomas Pollenus,UliègeAnne-CharlottePonsen,InsermU1197

Gury Popov,UniversityofSaint-PetersburgMichael Potente,MPIforHeart&LungResearchSimoneReginaPotje,UniversityofSãoPauloJutta Poutanen,HerantisPharmaPlcSaurabh Prabhu,UniversityofEastAngliaMarc Praetner,Walter-Brendel-CentreMarc Pritzker,UniversityofMinnesotaBartosz Proniewski,JagiellonianUniversityMeiyu Qiu,IBSSusan Quaggin,NorthwesternUniversityPatrick Quaggin-Smith,ManninResearchShahin Rafii,WeillCornellMedicineBrian Raftrey,StanfordUniversityMohanraj Ramachandran,UppsalaUniversityChristian Ramakers,MimetasDamien Ramel,InsermAnna Randi,ImperialCollegeLondonVoahanginirinaRandriamboavonjy,GoetheUniversityRisto Ranta,PromocellGmbh/BiotopOyKrista Rantanen,Svanholm.comApsJulien Ratelade,InsermAngela Raucci,CentroCardiologicoMonzinoKhushbu Rauniyar,UniversityofHelsinkiDhanya Ravindran,HeartResearchInstituteAarthi Ravindran,UniversityofEasternFinlandDino Ravnic,PennStateUniversityLaurence Rayssinguier,FujifilmVisualsonicsAnton Razuvaev,KarolinskaInstitutetKristy Red-Horse,StanfordUniversityDaniela Regensburger,UK-ErlangenVéronique Regnault,InsermU1116Sonia Rehal,MSKCCTore Reikvam,UniversityOfBergenYvonne Reiss,GoetheUniversityHospitalMarie-Ange Renault,InsermChristian Renken,AppliedBiophysicsWilliam Repicci,LE&RNChris Reutelingsperger,UniversityMaastrichtJordi Ribera-Sabate,IdibapsMark Richards,UppsalaUniversityAdrian Rodriguez-Contreras,CityUniversitytofNewYorkJesusEduardoRojoArias,TUDresdenCharlotteRorsman,UppsalaUniversityAndre Rosa,MDCforMolecularMedicineJane Roscoe,BioscientificaDror Rosenbach,WeizmannInstituteofScienceElisa Rossi,InsermUMR_S1140Lise Roth,EmboPressMichaela Roth,LundUniversityAleksandra Rovnaia,StPetersburgMedicalUniversityAnna-KaisaRuotsalainen,UniversityofEasternFinlandGiusy Russomanno,ImperialCollegeLondonMaija Ruuth,WihuriResearchInstituteMichael Ryczko,ManninResearchCurzio Rüegg,UniversityofFribourgUrszula Rykaczewska,KarolinskaInstitutetJuhee Ryu,ChonnamNationalUniversityJiKan Ryu,InhaUniversityMarkus Räsänen,WihuriResearchInstituteLigia SBBoisserand,YaleUniversityAnne Saarikko,HelsinkiUniversityHospitalPipsa Saharinen,UniversityofHelsinkiCecilia Sahlgren,ÅboAkademiAnneleSainio,UniversityofTurkuMiguel Sainz-Jaspeado,UppsalaUniversityAntonija Sakic,UniversityofGeneva

Posters – Monday

– 212 –

IVBM2018

Nagisa Sakurai,AstellasInstitutePäivi Salminen,HelsinkiUniversityHospitalTuire Salonurmi,UniversityofOuluMaryna Samus,MPIforMolecularBiomedicineMasaki Sano,HamamatsuUniversityMike Sapieha,UniversityofMontrealKaisa Sarkkinen,UniversityofHelsinkiNorihiko Sasaki,TokyoMetropolitanInstituteSandro Satta,ManchesterMetUniversityMika Sawane,ShiseidoResearchCenterJohanna Schaffenrath,UniversityHospitalZürichMartin Schneider,EthZurichKlaudia Schossleitner,MedicalUniversityofViennaStefan Schulte-Merker,WwuMünsterLeon Schurgers,MaastrichtUniversityMartin Schwartz,YaleUniversityJulian Schwartze,UniversityofGlasgowKerstin Schäfer,MPIforMolecularBiomedicineMarcus Schäfer,nanoAnalyticsGmbHConcetta Scimone,UniversityofMessinaGiorgio Seano,InstitutCurieResearchCenterMarta Segarra,GoetheUniversityFrankfurtCédric Seignez,UppsalaUniversityTill Seime,KarolinskaInstitutetAnna Selmi,MedicalUniversityofLodzIlakya Selvarajan,UniversityofEasternFinlandWilliam Sessa,YaleUniversitySalim Seyfried,PotsdamUniversityApeksha Shapeti,KULeuvenNeha Sharma,MedicalUniversityofGrazSomanath Shenoy,UniversityofGeorgiaLingyan Shi,ColumbiaUniversityJingjing Shi,GermanCancerResearchCenterMasabumi Shibuya,JobuUniversityYoung-Joo Shin,InjeUniversityKeisuke Shirakura,OsakaUniversityArndt Siekmann,MPIforMolecularBiomedicineMichael Simons,YaleUniversityMahak Singhal,GermanCancerResearchCenterTuomas Sipilä,UniversityofHelsinkiMauro Siragusa,GoetheUniversityLaura Sironi,UniversityofMilano-BicoccaAllan Sirsjö,ÖrebroUniversityElinSjöberg,UppsalaUniversityMarika Sjöqvist,ÅboAkademiUniversityRenaeSkoczylas,UppsalaUniversityDavor Skofic-Maurer,MedicalUniversityofGrazGryFreja Skovsted,UniversityofCopenhagenSadie Slater,UniversityofBristolJudith Sluimer,MaastrichtUniversityNicola Smart,UniversityofOxfordMarta Smeda,JagiellonianUniversityIlya Smirnov,RussianResearchCenterKerrie Smith,UniversityofLeedsRoss Smith,UppsalaUniversityMarloes Sol,UniversityMedicalCenterGRFabrice Soncin,Cnrs-umr8161Iguaracy Sousa,UniversityofSãoPauloDidier Stainier,MPIforHeart&LungResearchJimmyStalin,UniversityofFribourgRadu Stan,GeiselSchoolofMedicineBrina Stancic,UppsalaUniversityLaura Stanicek,VUMedicalCenterAmsterdamTheresa Staniczek,HeidelbergUniversityChristina Stefanitsch,KarolinskaInstitutetMagdalena Sternak,JagiellonianUniversity

Heike Stingl,InstituteForVascularSignallingMarta Stojak,JagiellonianUniversityAnastasia Stolbovaya,RussianResearchCenterEike Struck,TRECwonhee Suh,Chung-AngUniversityPaula Summanen,HelsinkiUniversityHospitalVeronica Sundell,UppsalaUniversityJinyoung Sung,YeungnamUniversityJoanna Suraj,JagiellonianUniversityBianca Suur,KarolinskaInstitutetNakoMaffoSuzanneOlive,AtlanticMedicalCentreBent Svanholm,Svanholm.comApSSteven Swendeman,BostonChildren’sHospitalDánielImre Szőke,SemmelweisUniversityAndrea Szuchman-Sapir,MIGAL-GalileeResearchInstituteRobert Szulcek,VUMedicalCenterAmsterdamSina Tadayon,UniversityofTurkuIkue Tai-Nagara,KeioUniversityNobuyuki Takakura,OsakaUniversityAkira Takeda,UniversityofTurkuNaoko Takubo,UniversityOfTokyoSara Tamagno,UniversityofEdinburghWaiho Tang,GuangzhouMedicalCentreJayendrakishoreTanjoreRamanathan,UniversityofHelsinkiAnuradha Tarafdar,UniversityofExeterClaire Tardiveau,IPBSMarja-Riitta Taskinen,UniversityofHelsinkiDenise Teber,MPIforMolecularBiomedicineTambet Teesalu,UniversityofTartuInes TelesSiefersAlves,SpringerNatureHanoch Tempelhof,WeizmannInstituteofScienceFabian Tetzlaff,GermanCancerResearchCenterYaara Tevet,WeizmannInstituteJérémy Thalgott,LUMCPierre-Louis Tharaux,InsermJean-Leon Thomas,InsermHannah Thomas,UniversityofSouthAustraliaDurgaDevi Thota,UniversityofEasternFinlandGavin Thurston,RegeneronPharmaceuticalsEmmi Tiilikainen,UniversityofHelsinkiSaara Tikka,PfizerOyKaKa Ting,CentenaryInstituteAnnakaisa Tirronen,UniversityofEasternFinlandEugene Tkachenko,UCSDDebbie Toburen,3scanTarja Toimela,UniversityofTampereMateusz Tomczyk,JagiellonianUniversityAnu Toropainen,UniversityofEasternFinlandVerónica Torres,CatholicUniversityofChileMartina Trávníčková,CzechAcademyofSciencesRoman Tsaryk,MPIforMolecularBiomedicineMarianna Tsifaki,Queen’sUniversityBelfastMaria Tsioumpekou,UppsalaUniversityYohei Tsukada,OsakaUniversityRiikka Tulamo,HelsinkiUniversityHospitalTimo Tumelius,LabemaOySarka Tumova,UniversityofHelsinkiPatric Turowski,UclInstituteOfOphthalmologyOrsolya Török,UniversityHospitalZürichMaria Ulvmar,UppsalaUniversityKari Vaahtomeri,UniversityofHelsinki&WRIAlessandra Vaccaro,UppsalaUniversityMathew Vadas,CentenaryInstituteGudrun Valdimarsdottir,UniversityofIcelandJaap VanBuul,SanquinResearchMaureen VanDeVelde,UniversityofLiège,GIGA-Cancer

Participants

Posters – Monday

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IVBM2018

BernardVanDenBerg,LeidenUniversityMedicalCenterCharissa vandenBrom,VUMedicalCenterAmsterdamMartijn VanDerEnt,UniversityofMichiganAnne-Eva VanDerWijk,AcademicMedicalCenterJanine VanGils,LeidenUniversityMedicalCenterRick VanGorp,CarimVictor VanHinsbergh,VUMedicalCenterAmsterdamLuuk VanHooren,UppsalaUniversityKim VanKuijk,MaastrichtUniversityMax VanLessen,UniversityofMünsterMatijs VanMeurs,UmcgHans VanOosterwyck,KULeuvenBram VanSteen,SanquinResearchMichael Vanlandewijck,KarolinskaInstitutetAlejandra VargasValderrama,InsermU1197Sara Vasconcelos,UniversityHealthNetworkKalyani Vemuri,UppsalaUniversityLakshmi Venkatraman,UppsalaUniversityAline Verstraeten,UniversityofAntwerpDietmar Vestweber,MPIforMolecularBiomedicineMiikka Vikkula,UniversiteCatholiquedeLouvainAnne-Clemence Vion,MDCforMolecularMedicineSibylle VonVietinghoff,HannoverMedicalSchoolTaina Vuorio,UniversityofEasternFinlandMaria Vähätupa,UniversityofTampereTaku Wakabayashi,OsakaUniversityKenneth Walsh,BostonUniversityLi Wan,NanjingUniversityGangqi Wang,LeidenUniversityMedicalCenterShengpeng Wang,MPIforHeart&LungResearchNeleWarmke,UniversityofLeedsTetsuro Watabe,TokyoMedical&DentalUnivMasafumi Watanabe,YamagataUniversityHerbert Weich,HelmholtzCentreJanine Weis,UniversityofHelsinkiJakob Weissenberger,EdingerInstituteGili Wellner,WeizmannInstituteLinqian Weng,KULeuvenAnn-Cathrin Werner,LMUMunichEleonoora Wihuri,WihuriResearchInstituteHelge Wiig,UniversityofBergenKerstin Wilhelm,MPIforHeart&LungResearchAnnalenaWille,UppsalaUniversityAriel Wilson,Maisonneuve-RosemontCenterJörg Wilting,UniversityofGöttingenManuel Winkler,HeidelbergUniversityGalina Wirth,UniversityofEasternFinlandSofia Wittgren,KarolinskaInstitutetSebastian Wohlfeil,HeidelbergUniversityBeata Wojciak-Stothard,ImperialCollegeLondonBingruo Wu,AlbertEinsteinCollegeHao Wu,BostonChildren’sHospitalMei Xin,CincinnatiChildren’sHospitalSeiji Yamamoto,UniversityofToyamaJun Yamashita,KyotoUniversityGuangyao Yan,LudwigMaximiliansUniversityMyungJin Yang,IBSJeeMyung Yang,KAISTJiHun Yang,KoreaUniversityHanMo Yang,SeoulNationalUniversityKarina Yaniv,WeizmannInstituteofScienceAnthony Yau,UppsalaUniversity

KimPin Yeo,NUSShaw-Fang Yet,NatHealthResearchInstitutesJiang Yin,AlbertaLymphedemaNetworkGuoNan Yin,InhaUniversityXiangke Yin,SunYat-senUniversitySeppo Ylä-Herttuala,UniversityofEasternFinlandKyungsang Yoo,KyungHeeUniversityMasayuki Yoshida,TokyoMedical&DentalUnivYasuhiro Yoshimatsu,TokyoMedical&DentalUnivLee YouMie,KyungpookNationalUniversityWei Yu,ChineseAcademyofSciencesJun Yu,TempleUniversityPengchun Yu,YaleUniversityIan Zachary,UniversityCollegeLondonGeorgia Zarkada,YaleUniversityMulugeta Zegeye,ÖrebroUniversityManuelZeitelhofer,KarolinskaInstitutetZhi Zeng,GuangzhouMedicalCentreZheng Zhang,RegeneronPharmaceuticalsYan Zhang,UppsalaUniversityYang Zhang,UppsalaUniversityYang Zhao,CentenaryInstituteQi Zhao,RegeneronPharmaceuticalsXiaocheng Zhao,VibBin Zhou,AlbertEinsteinCollegeBin Zhou,ChineseAcademyofSciencesFei Zhou,SoochowUniversityChangcheng Zhou,UniversityofKentuckyWenping Zhou,YaleUniversityWendy Zhu,UniversityofUtahJan Zijlstra,UniversityMedicalCenterGRBerislav Zlokovic,KeckSchoolofMedicineEstella Zuccolo,CentroCardiologicoMonzinoPeter Zwiers,UniversityMedicalCenterGRAn Zwijsen,KULeuvenTiit Örd,UniversityofEasternFinlandKatariina Öörni,WihuriResearchInstitute

Participants

international vascular biology meeting 2018 · unique portfolio of bioluminescent cell lines and ˜...

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