Eur Rev Med Pharmacol Sci 2018; 22 (7): 2077-2083

DOI: 10.26355/eurrev_201804_14739

MicroRNA-194 participates in endotoxemia induced myocardial injury via promoting apoptosis

Y. Zhai, N. Ding

Health Management Division, The People’s Hospital of Weifang, Weifang, Shandong, China. ddnn-0057@163.com


OBJECTIVE: To investigate the expression level of microRNA-194 in myocardial injury induced by lipopolysaccharide (LPS) and its underlying mechanism.

MATERIALS AND METHODS: LPS-induced H9c2 cardiomyocytes injury model was established. The expression level of microRNA-194 at different treatment time points was detected. Survival and apoptosis of cardiomyocytes were detected after overexpression or knockdown of microRNA-194. The target genes of microRNA-194 were predicted by bioinformatics analysis. The relationship between microRNA-194 and target genes was verified by the dual luciferase reporter analysis and Western blot. The effects of microRNA-194 mimics and overexpression plasmid pcDNA3/Slc7a5 on the cardiomyocyte apoptosis were investigated by MTT assay. Expressions of relative genes involved in Wnt/β-catenin pathway during the process of LPS-induced cardiomyocytes injury were detected by qRT-PCR and Western blot.

RESULTS: The expression level of microRNA-194 was increased in LPS-induced H9c2 cardiomyocytes injury model in a time-dependent manner. Overexpressed microRNA-194 directly bound to the target gene Slc7a5 and inhibited its expression. Transfection of microRNA-194 mimics increased apoptosis of H9c2 cells, which was rescued by overexpression of pcDNA3/Slc7a5. MicroRNA-194 was capable of promoting cardiomyocyte apoptosis by activating Wnt/β-catenin pathway.

CONCLUSIONS: MicroRNA-194 promotes cardiomyocyte apoptosis and participates in myocardial injury induced by endotoxemia via activating Wnt/β-catenin pathway.

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To cite this article

Y. Zhai, N. Ding
MicroRNA-194 participates in endotoxemia induced myocardial injury via promoting apoptosis

Eur Rev Med Pharmacol Sci
Year: 2018
Vol. 22 - N. 7
Pages: 2077-2083
DOI: 10.26355/eurrev_201804_14739