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

Abstract

To investigate the expression level of microRNA-194 in myocardial injury induced by lipopolysaccharide (LPS) and its underlying mechanism. 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. 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. MicroRNA-194 promotes cardiomyocyte apoptosis and participates in myocardial injury induced by endotoxemia via activating Wnt/β-catenin pathway.