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microRNA‐193b protects against myocardial ischemia‐reperfusion injury in mouse by targeting mastermind‐like 1
Author(s) -
Zhang Jinzhu,
Niu Jingjing,
Tian Baoqing,
Zhao Meng
Publication year - 2019
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.28684
Subject(s) - microrna , myocardial ischemia , ischemia , reperfusion injury , medicine , pharmacology , microbiology and biotechnology , cardiology , chemistry , biology , biochemistry , gene
Abstract The current study aimed to explore the functions and roles of microRNA‐193b (miR‐193b) in the myocardium with ischemia‐reperfusion (I/R) injury and a potential therapeutic method for myocardial I/R injury. The mice were subjected to myocardial I/R with or without miR‐193b pretreatment. The infarct size and myocardial enzymes were detected. The terminal deoxynucleotidyl transferase dUTP nick‐end labeling assay was conducted to investigate the effect of miR‐193b on cardiomyocyte apoptosis. The expression levels of miR‐193b and mastermind‐like 1 (MAML1) were validated by quantitative real‐time polymerase chain reaction and Western blot analysis. The results suggested that the miR‐193b expression level was significantly downregulated in the myocardium with I/R injury compared with control group. miR‐193b overexpression is able to reduce infarct size and myocardial enzymes after myocardial I/R injury. Furthermore, overexpression of miR‐193b could alleviate the apoptosis level after myocardial I/R injury. Taken together, the present study demonstrated that upregulated miRNA‐193b alleviated myocardial I/R injury via targeting MAML1.