期刊
ASIAN PACIFIC JOURNAL OF TROPICAL MEDICINE
卷 8, 期 9, 页码 732-736出版社
WOLTERS KLUWER MEDKNOW PUBLICATIONS
DOI: 10.1016/j.apjtm.2015.07.023
关键词
MicroRNA-208a; Apoptosis; Cardiomyocytes; Mitochondrial fission
资金
- Shandong Natural Science Fund [ZR2009CL018]
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.
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