| Literature DB >> 31618500 |
Duomao Lin1, Boqun Cui1, Jun Ma1, Jiayue Ren1.
Abstract
MicroRNAs have been reported to be implicated in myocardial ischemia/reperfusion (I/R) injury. The purpose of this study was to investigate the effect of miR-183-5p on I/R injury. Overexpression of miR-183-5p by agomiR transfection alleviated cardiac dysfunction and significantly reduced the infarct size in rats with myocardial I/R. MiR-183-5p also alleviated myocardial apoptosis with reduced apoptotic cells and lower levels of apoptosis associated proteins. in vitro experiments were conducted on rat H9c2 cells treated with anoxia/reoxygenation (A/R). Annexin V/propidium iodide (PI) staining and flow cytometry reported that the ratio of apoptotic cells decreased by miR-183-5p transfection before A/R treatment. Moreover, according to binding sequence prediction and Dual luciferase reporter assay, we explored that voltage-dependent anion channel 1 (VDAC1), which aggravates myocardial injury and apoptosis reported in our former research, was a target of miR-183-5p. In conclusion, miR-183-5p can efficiently attenuate I/R injury and miR-183-5p may exert its effect through repressing VDAC1 expression.Entities:
Keywords: H9c2 cells; ischemia/reperfusion injury; microRNA-183-5p; rat; voltage-dependent anion channel 1
Year: 2019 PMID: 31618500 DOI: 10.1002/biof.1571
Source DB: PubMed Journal: Biofactors ISSN: 0951-6433 Impact factor: 6.113