Journal
BIOFACTORS
Volume 46, Issue 1, Pages 83-93Publisher
WILEY
DOI: 10.1002/biof.1571
Keywords
H9c2 cells; ischemia; reperfusion injury; microRNA-183-5p; rat; voltage-dependent anion channel 1
Funding
- Beijing Hospitals Authority Youth Programme [QML 20180602]
- Beijing Municipal Administration of Hospitals' Clinical Medicine Development of Special Funding Support [ZYLX201810]
- National Natural Science Foundation of China [81471902, 81871592]
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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.
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