Downregulation MicroRNA-1 Can Protect H2O2 Injured Cardiomyocytes
10.3969/j.issn.0253-9896.2014.08.001
- VernacularTitle:下调microRNA-1对H2O2诱导的心肌细胞损伤的保护作用
- Author:
Junyi ZHENG
;
Ying CAI
;
Hongliang CONG
;
Jin ZHOU
- Publication Type:Journal Article
- Keywords:
microRNAs;
myocytes,cardiac;
apoptosis;
transfection;
oxidative stress;
hydrogen peroxide;
miR-1
- From:
Tianjin Medical Journal
2014;(8):737-740
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective function and mechanism of microRNA-1 (miR-1) downregula-tion in H2O2 injured cardiomyocytes. Methods The experiment was divided into 4 groups:Blank group, Negative Control group (NC), H2O2 group and H2O2+AS-miR-1 group. Cells in blank group were not underwent any treatment. Cells in NC group were transfected with random miRNA fragment. H2O2 and H2O2+AS-miR-1 groups were defined as H2O2 injured car-diomyocytes without or with transfected antisense miR-1 oligonucleotide(AS-miR-1). Real time PCR was used to test miR-1 transcription level, and cell vitality and apoptosis were analyzed by MTT and flow cytometry. The target gene of miR-1 was predicted by bioinformatics, then its mRNA transcription and protein expression level of Bcl-2 were detected by real time PCR and western blot respectively. Results There is no significant difference of all index between Blank group and NC group. H2O2 can induce cardiomyocyte injury, increase miR-1 level and rise apoptosis rate, reduce cell vitality and de-crease Bcl-2 expression level. Transfection of AS-miR-1 can decrease cell apoptosis, increase cell vitality and enhance Bcl-2 expression level. Conclusion Downregulation of microRNA-1 can protect cardiomyocytes that was injured by H2O2 through increasing anti-apoptosis factor Bcl-2 expression.
