miR-27a-5p Attenuates Hypoxia-induced Rat Cardiomyocyte Injury by Inhibiting Atg7

International Journal of Molecular Sciences

Surong Shuai¹  Keren Long¹  Li Zhu¹  Wanling Qiu¹  Yujie Wang¹  Qianzi Tang¹  Zihui Hu¹  Xun Wang¹  Jideng Ma¹  Long Jin¹  Xuewei Li¹  Jinwei Zhang¹  Guoqing Tang¹  Mingzhou Li¹ 

[1] Institute of Animal Genetics and Breeding, College of Animal Science and Technology, Sichuan Agricultural University, Chengdu 611130, Sichuan, China;

关键词: miR-27a-5p;    acute myocardial infarction;    autophagy;    apoptosis;    hypoxia;   

DOI  :  10.3390/ijms20102418

来源: DOAJ

【 摘 要 】

Acute myocardial infarction (AMI) is an ischemic heart disease with high mortality worldwide. AMI triggers a hypoxic microenvironment and induces extensive myocardial injury, including autophagy and apoptosis. MiRNAs, which are a class of posttranscriptional regulators, have been shown to be involved in the development of ischemic heart diseases. We have previously reported that hypoxia significantly alters the miRNA transcriptome in rat cardiomyoblast cells (H9c2), including miR-27a-5p. In the present study, we further investigated the potential function of miR-27a-5p in the cardiomyocyte response to hypoxia, and showed that miR-27a-5p expression was downregulated in the H9c2 cells at different hypoxia-exposed timepoints and the myocardium of a rat AMI model. Follow-up experiments revealed that miR-27a-5p attenuated hypoxia-induced cardiomyocyte injury by regulating autophagy and apoptosis via Atg7, which partly elucidated the anti-hypoxic injury effects of miR-27a-5p. Taken together, this study shows that miR-27a-5p has a cardioprotective effect on hypoxia-induced H9c2 cell injury, suggesting it may be a novel target for the treatment of hypoxia-related heart diseases.

【 授权许可】

Unknown