ABSTRACT
Mitochondriamediated apoptosis is the primary cause of cardiomyocyte death. Therefore, mitochondria are a key target for treating myocardial injury. Mitochondrial calcium uniporter regulator 1 (MCUR1)mediated mitochondrial calcium homeostasis markedly promotes cell proliferation and resistance to apoptosis. However, whether MCUR1 is involved in regulation of cardiomyocyte apoptosis during myocardial ischaemiareperfusion remains unknown. microRNA124 (miR124) is upregulated in cardiovascular disease, suggesting a key role for miR124 in the cardiovascular system. Whether miR124 affects cardiomyocyte apoptosis and myocardial infarction is not well understood. Western blot showed that miR124 and MCUR1 were upregulated in cardiomyocyte apoptosis induced by hydrogen peroxide (H2O2). Flow cytometry assay of cell apoptosis showed that miR124 inhibited cardiomyocyte apoptosis by activating MCUR1 following H2O2 treatment. The dualluciferase reporter assay confirmed binding of miR124 to MCUR1 3'UTR and subsequent activation of MCUR1. FISH assay revealed the entry of miR124 into the cell nucleus. Therefore, MCUR1 was identified as a novel target of miR124, and it was shown that the miR124MCUR1 axis modulated cardiomyocyte apoptosis induced by H2O2 in vitro. The results indicated induced expression of miR124 during acute myocardial infarction and its transport to the nucleus. In the nucleus, miR124 transcriptionally activated MCUR1 by binding to its enhancers. These findings reveal a role of miR124 as a biomarker for myocardial injury and infarction.