MicroRNA-590-3p relieves hypoxia/reoxygenation induced cardiomyocytes apoptosis and autophagy by targeting HIF-1α

MicroRNA-590-3p 通过靶向 HIF-1α 缓解缺氧/复氧诱导的心肌细胞凋亡和自噬

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作者:Nengjing Gong, Xiaohuai Yang, Xiaoyu Li, Yuyu Jiang, Cuifang Gu, Shasha Ma, Qin Gao, Xiangyang Cheng

Abstract

Autophagy and apoptosis are key factors in myocardial ischemia/reperfusion (I/R) injury. MicroRNAs (miRNAs or miRs) participate in occurrence and development of myocardial I/R injury by regulating autophagy and apoptosis. The purpose of the present study was to investigate the role of miR-590-3p in the regulation of autophagy and apoptosis in hypoxia/reoxygenation (H/R)-treated cardiomyocytes. Following 6 h hypoxia and 6 h reoxygenation in primary rat cardiomyocytes, miR-590-3p was downregulated. Transfection of miR-590-3p mimic inhibited the increased autophagy and apoptosis following H/R treatment. Subsequent experiments demonstrated that miR-590-3p regulated induction of autophagy and apoptosis by targeting hypoxia inducible factor (HIF)-1α. Forced expression of HIF-1α rescued the protective effect of miR-590-3p on H/R-induced cardiomyocytes. In summary, the present study showed that miR-590-3p exhibited a protective effect on H/R-induced cardiomyocyte injury and may be a novel target for the treatment of myocardial ischemia disease.

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