Journal article
Role of the CD39/CD73 purinergic pathway in modulating arterial thrombosis in mice
R Covarrubias, E Chepurko, A Reynolds, ZM Huttinger, R Huttinger, K Stanfill, DG Wheeler, T Novitskaya, SC Robson, KM Dwyer, PJ Cowan, RJ Gumina
Arteriosclerosis Thrombosis and Vascular Biology | LIPPINCOTT WILLIAMS & WILKINS | Published : 2016
Abstract
Objective-Circulating blood cells and endothelial cells express ectonucleoside triphosphate diphosphohydrolase-1 (CD39) and ecto-5'-nucleotidase (CD73). CD39 hydrolyzes extracellular ATP or ADP to AMP. CD73 hydrolyzes AMP to adenosine. The goal of this study was to examine the interplay between CD39 and CD73 cascade in arterial thrombosis. Approach and Results-To determine how CD73 activity influences in vivo thrombosis, the time to ferric chloride-induced arterial thrombosis was measured in CD73-null mice. In response to 5% FeCl3, but not to 10% FeCl3, there was a significant decrease in the time to thrombosis in CD73-null mice compared with wild-Type mice. In mice overexpressing CD39, abla..
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Awarded by National Institutes of Health
Funding Acknowledgements
This work was supported in part by the National Heart, Lung, and Blood Institute of the National Institutes of Health through training grant 5T32HL007411-35 to R. Covarrubias, R01-HL094400 to S.C. Robson and grants K08-HL094703 and R21-HL096038 to R.J. Gumina.