MiR‑124 inhibits cardiomyocyte apoptosis in myocardial ischaemia‑reperfusion injury by activating mitochondrial calcium uniporter regulator 1.

Abstract

Mitochondria‑mediated 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 ischaemia‑reperfusion remains unknown. microRNA‑124 (miR‑124) is upregulated in cardiovascular disease, suggesting a key role for miR‑124 in the cardiovascular system. Whether miR‑124 affects cardiomyocyte apoptosis and myocardial infarction is not well understood. Western blot showed that miR‑124 and MCUR1 were upregulated in cardiomyocyte apoptosis induced by hydrogen peroxide (H2O2). Flow cytometry assay of cell apoptosis showed that miR‑124 inhibited cardiomyocyte apoptosis by activating MCUR1 following H2O2 treatment. The dual‑luciferase reporter assay confirmed binding of miR‑124 to MCUR1 3'‑UTR and subsequent activation of MCUR1. FISH assay revealed the entry of miR‑124 into the cell nucleus. Therefore, MCUR1 was identified as a novel target of miR‑124, and it was shown that the miR‑124‑MCUR1 axis modulated cardiomyocyte apoptosis induced by H2O2 invitro. The results indicated induced expression of miR‑124 during acute myocardial infarction and its transport to the nucleus. In the nucleus, miR‑124 transcriptionally activated MCUR1 by binding to its enhancers. These findings reveal a role of miR‑124 as a biomarker for myocardial injury and infarction.