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

被引：47

作者：

Zhang, Jinwei ^{[1
,2
]}

Qiu, Wanling ^{[1
,2
]}

Ma, Jideng ^{[1
,2
]}

Wang, Yujie ^{[1
,2
]}

Hu, Zihui ^{[1
,2
]}

Long, Keren ^{[1
,2
]}

Wang, Xun ^{[1
,2
]}

Jin, Long ^{[1
,2
]}

Tang, Qianzi ^{[1
,2
]}

Tang, Guoqing ^{[1
,2
]}

Zhu, Li ^{[1
,2
]}

Li, Xuewei ^{[1
,2
]}

Shuai, Surong ^{[1
,2
]}

Li, Mingzhou ^{[1
,2
]}

机构：

[1] Sichuan Agr Univ, Coll Anim Sci & Technol, Inst Anim Genet & Breeding, Chengdu 611130, Sichuan, Peoples R China

[2] Sichuan Agr Univ, Farm Anim Genet Resource Explorat & Innovat Key L, Chengdu 611130, Sichuan, Peoples R China

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2019年 / 20卷 / 10期

基金：

国家重点研发计划; 中国国家自然科学基金;

关键词：

miR-27a-5p; acute myocardial infarction; autophagy; apoptosis; hypoxia; H9C2; CELLS; EXCESSIVE AUTOPHAGY; APOPTOSIS; PROTECTS; CROSSTALK;

D O I：

10.3390/ijms20102418

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

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.

引用

页数：13