Evidence map›Paper›PMID 9077545›Full record

ArticleThe Journal of clinical investigation1997

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 and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
11.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

104 citing papers in PubMed, 407 citations in OpenAlex.

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44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

A J MarcusDepartment of Medicine, Veterans Affairs Medical Center, New York 10010-5050, USA. ajmarcus@mail.med.cornell.edu
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
C R Maliszewski
Cornell University · USAmgen (United States) · USVeterans Health Administration · US

Funding

Vascular signaling via scavenger receptorsP01HL046403 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI HAJJAR, KATHERINE AMBERSON · 1991 to 2011
$26.7M
NEW THROMBOREGULATORY PROTEIN, ANNEXIN IIR01HL042493 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI HAJJAR, KATHERINE AMBERSON · 1989 to 2016
$4.9M
Cell-Cell Interactions in Thrombosis -Request for Extension of Merit AwardR37HL047073 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI MARCUS, AARON JACOB · 2004 to 2011
$3.7M
Cell-Cell Interactions in Thrombosis -Request for Extension of Merit AwardR01HL047073 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DROSOPOULOS, JOAN H. F. · 1991 to 2014
$3.1M
NHLBI NIH HHS HL-42493NHLBI NIH HHS HL-46403NHLBI NIH HHS HL-47073
6 · The paper itself

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.

Indexed as

Adenosine TriphosphatasesAnimalsAntibodies, MonoclonalAntigens, CDApyraseCells, CulturedCOS CellsDNA, ComplementaryEndothelium, VascularEnzyme ActivationHumansIntracellular MembranesMicrosomesPlatelet Aggregation InhibitorsPrecipitin TestsRecombinant ProteinsAdenosine TriphosphatasesAntibodies, MonoclonalAntigens, CDApyraseCD39 antigenDNA, ComplementaryPlatelet Aggregation InhibitorsRecombinant ProteinsRNA, Messenger

Identifiers

PMID9077545
PMCPMC507951
OpenAlexW2002451448

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.