Effect of microRNA-208a on mitochondrial apoptosis of cardiomyocytes of neonatal rats
10.1016/j.apjtm.2015.07.023
- Author:
Ling-Dong MENG
1
;
Ru-Yi JIA
1
;
Ai-Chun MENG
2
;
Qing ZHU
3
;
Qing-Zan KONG
4
Author Information
1. Department of Cardiology, Second Affiliated Hospital of Taishan Medical University, Jinan No.4 People's Hospital
2. Department of Cardiology, Zhangqiu People's Hospital
3. Shandong Blood Center
4. Department of Cardiology, Affiliated Jinan Central Hospital of Shandong University
- Publication Type:Journal Article
- Keywords:
Apoptosis;
Cardiomyocytes;
MicroRNA-208a;
Mitochondrial fission
- From:
Asian Pacific Journal of Tropical Medicine
2015;8(9):747-751
- CountryChina
- Language:Chinese
-
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.
