Go to JCI Insight
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
  • Current issue
  • Past issues
  • By specialty
    • COVID-19
    • Cardiology
    • Gastroenterology
    • Immunology
    • Metabolism
    • Nephrology
    • Neuroscience
    • Oncology
    • Pulmonology
    • Vascular biology
    • All ...
  • Videos
    • Conversations with Giants in Medicine
    • Author's Takes
  • Reviews
    • View all reviews ...
    • Immune Environment in Glioblastoma (Feb 2023)
    • Korsmeyer Award 25th Anniversary Collection (Jan 2023)
    • Aging (Jul 2022)
    • Next-Generation Sequencing in Medicine (Jun 2022)
    • New Therapeutic Targets in Cardiovascular Diseases (Mar 2022)
    • Immunometabolism (Jan 2022)
    • Circadian Rhythm (Oct 2021)
    • View all review series ...
  • Viewpoint
  • Collections
    • In-Press Preview
    • Commentaries
    • Research letters
    • Letters to the editor
    • Editorials
    • Viewpoint
    • Top read articles
  • Clinical Medicine
  • JCI This Month
    • Current issue
    • Past issues

  • Current issue
  • Past issues
  • Specialties
  • Reviews
  • Review series
  • Conversations with Giants in Medicine
  • Author's Takes
  • In-Press Preview
  • Commentaries
  • Research letters
  • Letters to the editor
  • Editorials
  • Viewpoint
  • Top read articles
  • About
  • Editors
  • Consulting Editors
  • For authors
  • Publication ethics
  • Alerts
  • Advertising
  • Job board
  • Subscribe
  • Contact
Top
  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal
  • Top
  • Abstract
  • Version history
  • Article usage
  • Citations to this article

Advertisement

Research Article Free access | 10.1172/JCI119294

The endothelial cell ecto-ADPase responsible for inhibition of platelet function is CD39.

A J Marcus, M J Broekman, J H Drosopoulos, N Islam, T N Alyonycheva, L B Safier, K A Hajjar, D N Posnett, M A Schoenborn, K A Schooley, R B Gayle, and C R Maliszewski

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Marcus, A. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Broekman, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Drosopoulos, J. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Islam, N. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Alyonycheva, T. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Safier, L. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Hajjar, K. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Posnett, D. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Schoenborn, M. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Schooley, K. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Gayle, R. in: JCI | PubMed | Google Scholar

Department of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu

Find articles by Maliszewski, C. in: JCI | PubMed | Google Scholar

Published March 15, 1997 - More info

Published in Volume 99, Issue 6 on March 15, 1997
J Clin Invest. 1997;99(6):1351–1360. https://doi.org/10.1172/JCI119294.
© 1997 The American Society for Clinical Investigation
Published March 15, 1997 - Version history
View PDF
Abstract

We previously demonstrated that when platelets are in motion and in proximity to endothelial cells, they become unresponsive to agonists (Marcus, A.J., L.B. Safier, K.A. Hajjar, H.L. Ullman, N. Islam, M.J. Broekman, and A.M. Eiroa. 1991. J. Clin. Invest. 88:1690-1696). This inhibition is due to an ecto-ADPase on the surface of endothelial cells which metabolizes ADP released from activated platelets, resulting in blockade of the aggregation response. Human umbilical vein endothelial cells (HUVEC) ADPase was biochemically classified as an E-type ATP-diphosphohydrolase. The endothelial ecto-ADPase is herein identified as CD39, a molecule originally characterized as a lymphoid surface antigen. All HUVEC ecto-ADPase activity was immunoprecipitated by monoclonal antibodies to CD39. Surface localization of HUVEC CD39 was established by confocal microscopy and flow cytometric analyses. Transfection of COS cells with human CD39 resulted in both ecto-ADPase activity as well as surface expression of CD39. PCR analyses of cDNA obtained from HUVEC mRNA and recombinant human CD39 revealed products of the same size, and of identical sequence. Northern blot analyses demonstrated that HUVEC express the same sized transcripts for CD39 as MP-1 cells (from which CD39 was originally cloned). We established the role of CD39 as a prime endothelial thromboregulator by demonstrating that CD39-transfected COS cells acquired the ability to inhibit ADP-induced aggregation in platelet-rich plasma. The identification of HUVEC ADPase/CD39 as a constitutively expressed potent inhibitor of platelet reactivity offers new prospects for antithrombotic therapeusis.

Version history
  • Version 1 (March 15, 1997): No description

Article tools

  • View PDF
  • Download citation information
  • Send a comment
  • Share this article
  • Terms of use
  • Standard abbreviations
  • Need help? Email the journal

Metrics

  • Article usage
  • Citations to this article

Go to

  • Top
  • Abstract
  • Version history
Advertisement
Advertisement

Copyright © 2023 American Society for Clinical Investigation
ISSN: 0021-9738 (print), 1558-8238 (online)

Sign up for email alerts