[HTML][HTML] E-NTPDase1/CD39 modulates renin release from heart mast cells during ischemia/reperfusion: a novel cardioprotective role
The FASEB Journal, 2015•ncbi.nlm.nih.gov
Abstract Ischemia/reperfusion (I/R) elicits renin release from cardiac mast cells (MC), thus
activating a local renin-angiotensin system (RAS), culminating in ventricular fibrillation. We
hypothesized that in I/R, neurogenic ATP could degranulate juxtaposed MC and that ecto-
nucleoside triphosphate diphosphohydrolase 1/CD39 (CD39) on MC membrane could
modulate ATP-induced renin release. We report that pharmacological inhibition of CD39 in a
cultured human mastocytoma cell line (HMC-1) and murine bone marrow-derived MC with
activating a local renin-angiotensin system (RAS), culminating in ventricular fibrillation. We
hypothesized that in I/R, neurogenic ATP could degranulate juxtaposed MC and that ecto-
nucleoside triphosphate diphosphohydrolase 1/CD39 (CD39) on MC membrane could
modulate ATP-induced renin release. We report that pharmacological inhibition of CD39 in a
cultured human mastocytoma cell line (HMC-1) and murine bone marrow-derived MC with
Abstract
Ischemia/reperfusion (I/R) elicits renin release from cardiac mast cells (MC), thus activating a local renin-angiotensin system (RAS), culminating in ventricular fibrillation. We hypothesized that in I/R, neurogenic ATP could degranulate juxtaposed MC and that ecto-nucleoside triphosphate diphosphohydrolase 1/CD39 (CD39) on MC membrane could modulate ATP-induced renin release. We report that pharmacological inhibition of CD39 in a cultured human mastocytoma cell line (HMC-1) and murine bone marrow-derived MC with
ncbi.nlm.nih.gov
