MicroRNA-24 Inhibits Apoptosis Induced By Hypoxia In Cultured Cardiomyocytes

Ischemic/hypoxic myocardial injury is a major cause of cardiac dysfunction following myocardial infarction, which may eventually lead to heart failure. Exploring its action mechanism and looking for new therapeutic targets have therefore become major concerns of scientific research in this field. MicroRNAs (miRNAs) are a group of recently discovered small endogenous non-coding RNAs that regulate gene expression primarily through post-transcriptional repression or mRNA degradation in a sequence-specific manner. Ample evidence has shown that dysregulation of miRNA expression is associated with a variety of physiologic and/or pathophysiologic processes of the cardiovascular system, such as angiogenesis, arrhythmia, heart failure and cardiac hypertrophy. It was found in the present study that miRNAs were expressed aberrantly in the infarcted rat heart after coronary artery occlusion. Using microarray analysis and real-time PCR, we demonstrated for the first time that there were at least 8 miRNAs that were dysregulated due to hypoxia in the early stages of acute myocardial ischemia. Of these altered miRNAs, miR-24 was up-regulated in myocardial infarction. Overexpression of miR-24 in primary cultured cardiomyocytes inhibited hypoxia-induced apoptosis, and elimination of miR-24 by an antisense inhibitor exacerbated injury to cardiomyocytes. These findings suggest that miR-24 might play an essential role in ischemic and hypoxic myocardial injury-related heart diseases.