Research Papers:

MicroRNA-199a acts as a potential suppressor of cardiomyocyte autophagy through targeting Hspa5

Liang Chen, Fei-Yu Wang, Zhen-Yu Zeng, Ling Cui, Jian Shen, Xiao-Wei Song, Pan Li, Xian-Xian Zhao _ and Yong-Wen Qin

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Oncotarget. 2017; 8:63825-63834. https://doi.org/10.18632/oncotarget.19133

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Liang Chen1,2,*, Fei-Yu Wang1,*, Zhen-Yu Zeng1,*, Ling Cui3, Jian Shen1,4, Xiao-Wei Song1, Pan Li1, Xian-Xian Zhao1 and Yong-Wen Qin1

1Department of Cardiology, Changhai Hospital, Second Military Medical University, Shanghai 200433, China

2Department of Laboratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai 200433, China

3Department of Cardiology, People’s Hospital of Inner Mongolia, Hohhot 010017, China

4Department of Cardiology, 411 Hospital of PLA Navy, Shanghai 200081, China

*These authors have contributed equally to this work

Correspondence to:

Xian-Xian Zhao, email: [email protected]

Yong-Wen Qin, email: [email protected]

Keywords: microRNA, cardiomyocyte, autophagy, Hspa5

Received: August 31, 2016    Accepted: June 02, 2017    Published: July 10, 2017


Autophagy is an adaptive response to cardiomyocytes survival under stress conditions. MicroRNAs (miRNAs, miR) have been described to act as potent modulators of autophagy. To investigate whether and how miR-199a modulated autophagy in vitro, primary cardiomyocytes were treated under starvation to induce autophagy. Results showed that down-regulation of miR-199a was sufficient to activate cardiomyocytes autophagy. MiR-199a suppressed cardiomyocytes autophagy through direct inhibiting heat shock protein family A member 5 (Hspa5). Forced overexpression of Hspa5 recovered the inhibitory effect of miR-199a in autophagy activation. Our results suggested miR-199a as an effective suppressor of starvation-induced cardiomyocytes autophagy and that Hspa5 was a direct target during this process. These results extend the understanding of the role and pathway of miR-199a in cardiomyocytes autophagy, and may introduce a potential therapeutic strategy for the protection of cardiomyocytes in myocardial infarction or ischemic heart disease.

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