Downregulation of microRNA-100 protects H2O2-induced apoptosis in neonatal cardiomyocytes.

Hypoxia or reoxygenation-induced cardiomyocyte apoptosis is one of the major causes of cardiac dysfunction. Recently, regulations of microRNAs were shown to play important roles in cardiomyocyte apoptosis. MicroRNA-100 (miR-100) is one of the cardiac miRNA that was up-regulated in failing heart. In this study, we identified that miR-100 expression was up-regulated in H2O2-induced apoptosis in neonatal mice cardiomyocytes in a time-dependent manner. Furthermore, functional analysis revealed that miR-100 downregulation attenuated H2O2-induced apoptosis. Through biochemical analysis of western blot, we found that miR-100 suppressed the expression of insulin-like growth factor 1 receptor (IGF1R) during the process of hypoxia-induced apoptosis in cardiomyocytes. More importantly, ectopic down-regulation of IGF1R reversed the protective effect of miR-100 down-regulation on H2O2-induced apoptosis, revealing that miR-100 regulates cardiomyocyte apoptosis through the association of IGF1R. Taken together, our data demonstrated the functional role miR-100 in H2O2-induced apoptosis in cardiac dysfunctions.

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