Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats

Ling-Dong Meng; Ai-Chun Meng; Qing Zhu; Ru-Yi Jia; Qing-Zan Kong

doi:10.1016/j.apjtm.2015.07.023

Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats

Asian Pac J Trop Med. 2015 Sep;8(9):747-51. doi: 10.1016/j.apjtm.2015.07.023. Epub 2015 Jul 30.

Authors

Ling-Dong Meng¹, Ai-Chun Meng², Qing Zhu³, Ru-Yi Jia¹, Qing-Zan Kong⁴

Affiliations

¹ Department of Cardiology, Second Affiliated Hospital of Taishan Medical University, Jinan No.4 People's Hospital, Ji'nan 250031, Shandong, China.
² Department of Cardiology, Zhangqiu People's Hospital, Zhangqiu 250200, Shandong, China.
³ Shandong Blood Center, Ji'nan 250014, Shandong, China.
⁴ Department of Cardiology, Affiliated Jinan Central Hospital of Shandong University, Ji'nan 250014, Shandong, China. Electronic address: kongqingzanyisheng@163.com.

PMID: 26433661
DOI: 10.1016/j.apjtm.2015.07.023

Abstract

Objective: To explore the effect and mechanism of microRNA-208a (miR-208a) in the mitochondrial apoptosis of cardiomyocytes of neonatal rats.

Methods: The primary cultured cardiomyocytes of neonatal rats were added into the hypoxia incubator for the hypoxia induction. The overexpression system for miR-208a of cardiomyocytes of neonatal rats was built. The flow cytometry assay was employed to detect the incidence of apoptosis in the over-expressed miR-208a. The mitochondrial staining technique was used to detect the change in the mitochondrial morphology of over-expressed miR-208a. The bioinformatic analysis was chosen to analyze and predict the target gene of miR-208a.

Results: Firstly, the primary culture system of cardiomyocytes of neonatal rats was successfully built. The miR-208a was over-expressed in cardiomyocytes of neonatal rats by miR-208a Mimics. Results of flow cytometry assay showed that the over-expressed miR-208a could significantly reduce the incidence of apoptosis; while results of mitochondrial staining indicated the change in the mitochondrial morphology of over-expressed miR-208a and the mitochondrial fission process was inhibited. In conclusion, it was supposed that miR-208a could inhibit the activation of mitochondrial fission process to keep the cardiomyocytes from apoptosis.

Conclusions: The over-expressed miR-208a can reduce the incidence of apoptosis in the cardiomyocytes of neonatal rats, significantly change the mitochondrial morphology and inhibit the mitochondrial fission process.

Keywords: Apoptosis; Cardiomyocytes; MicroRNA-208a; Mitochondrial fission.