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MiR‐183‐5p protects rat hearts against myocardial ischemia/reperfusion injury through targeting VDAC1
Author(s) -
Lin Duomao,
Cui Boqun,
Ma Jun,
Ren Jiayue
Publication year - 2019
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1571
Subject(s) - vdac1 , propidium iodide , apoptosis , annexin , transfection , reperfusion injury , flow cytometry , microrna , ischemia , medicine , cardioprotection , pharmacology , chemistry , microbiology and biotechnology , biology , immunology , programmed cell death , biochemistry , gene , bacterial outer membrane , escherichia coli
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.