Ectonucleotidase CD39-driven control of postinfarction myocardial repair and rupture.

ABSTRACT: Mechanical complications of myocardial infarction (MI) are often fatal. Little is known about endogenous factors that predispose to myocardial rupture after MI. Ectonucleoside triphosphate diphosphohydrolase (CD39) could be a critical mediator of propensity to myocardial rupture after MI due to its role in modulating inflammation and thrombosis. Using a model of permanent coronary artery ligation, rupture was virtually abrogated in cd39^-/- mice versus cd39^+/+ controls, with elevated fibrin and collagen deposition and marked neutrophil and macrophage influx. Macrophages were found to display increased surface expression of CD301 and CD206, marking a reparative phenotype, driven by increased extracellular ATP and IL-4 in the infarcted myocardium of cd39

SUBMITTER: Sutton NR 

PROVIDER: S-EPMC5213916 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature