miR-192-5p mediates hypoxia/reoxygenation-induced apoptosis in H9c2 cardiomyocytes via targeting of FABP3.

Myocardial ischemia/reperfusion (I/R) injury is a leading cause of morbidity and mortality. In this study, we investigated the role of miR-192-5p in hypoxia/reoxygenation (H/R)-induced cardiomyocyte apoptosis. H9c2 cardiomyocytes were subjected to H/R and tested for miR-192-5p expression. Overexpression and knockdown experiments were performed to determine the effects of manipulating miR-192-5p on apoptotic responses. H/R-treated H9c2 cells exhibited a 2.2-fold increase in miR-192-5p levels. Overexpression of miR-192-5p significantly augmented apoptosis in H9c2 cells after H/R, which was accompanied by a significant increase in the ratio of Bax/Bcl-2. In contrast, delivery of anti-miR-192-5p inhibitors significantly reduced apoptosis induced by H/R. FABP3 was identified to be a functional target of miR-192-5p. Restoration of FABP3 prevented apoptosis in miR-192-5p-transfected H9c2 cells, whereas downregulation of FABP3 enhanced apoptosis in H/R-exposed H9c2 cells. In conclusion, miR-192-5p mediates H/R-induced apoptosis in cardiomyocytes by targeting FABP3 and represents a potential target for prevention of myocardial I/R injury.