Cd39 as a critical ectonucleotidase defense against pathological vascular remodeling.

CD39 AS A CRITICAL ECTONUCLEOTIDASE DEFENSE AGAINST PATHOLOGICAL VASCULAR REMODELING. Trans Am Clin Climatol Assoc. 2018;129:132-139 Authors: Pinsky DJ Abstract A common thread underlying vascular or tissue injury is the loss of plasmalemmal integrity and the passive (or even active) spillage of intracellular contents into the circulation. Purinergic nucleotides, which serve as energy shuttling moieties within cells, are among the contents released into the bloodstream, where they signal danger and trigger thrombosis and inflammation. To regain vascular homeostasis, vascular cells have evolved highly conserved mechanisms to transact the catalytic degradation of extracellular nucleotides such as adenosine triphosphate (ATP) and adenosine diphosphate (ADP). CD39, the main endothelial ectonucleotidase which cleaves ATP and ADP, plays an essential role in ridding the bloodstream of these danger signals, thereby sustaining vascular homeostasis. Studies herein describe the upregulation of endothelial CD39 gene by steady laminar shear forces, and conversely, its downregulation under turbulent flow conditions. CD39 appears to be a critical ectonucleotidase which suppresses atherogenesis under experimental hyperlipidemic conditions in mice, and which also significantly mitigates pathologic vascular remodeling and development of pulmonary arterial hypertension in mice placed under chronic hypoxic conditions. Together, these data reveal that CD...
Source: Transactions of the American Clinical and Climatological Association - Category: General Medicine Tags: Trans Am Clin Climatol Assoc Source Type: research