Targeted disruption of cd39/ATP diphosphohydrolase results in disordered hemostasis and thromboregulation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1999-09

AUTHORS

Keiichi Enjyoji, Jean Sévigny, Yuan Lin, Paul S. Frenette, Patricia D. Christie, Jan Schulte Am Esch, Masato Imai, Jay M. Edelberg, Helen Rayburn, Miroslaw Lech, David L. Beeler, Eva Csizmadia, Denisa D. Wagner, Simon C. Robson, Robert D. Rosenberg

ABSTRACT

CD39, or vascular adenosine triphosphate diphosphohydrolase, has been considered an important inhibitor of platelet activation. Unexpectedly, cd39-deficient mice had prolonged bleeding times with minimally perturbed coagulation parameters. Platelet interactions with injured mesenteric vasculature were considerably reduced in vivo and purified mutant platelets failed to aggregate to standard agonists in vitro. This platelet hypofunction was reversible and associated with purinergic type P2Y1 receptor desensitization. In keeping with deficient vascular protective mechanisms, fibrin deposition was found at multiple organ sites in cd39-deficient mice and in transplanted cardiac grafts. Our data indicate a dual role for adenosine triphosphate diphosphohydrolase in modulating hemostasis and thrombotic reactions. More... »

PAGES

1010

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/12447

DOI

http://dx.doi.org/10.1038/12447

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1013810589

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10470077


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