Objectives To explore the effect and mechanism of microRNA(miR)-208a-3p on cardiac hypertrophy(CH)after myocardial infarction(MI)by targeting GATA4 expression in mice.Methods Mice were divided into control group,MI group,MI+miR-208a-3p inhibitor group(n=12).CH model was built by ligation.MiR-208a-3p was inhibited by intravenous injection of miR-208a-3p inhibitor(300 μg).Heart mass(HM,mg)/tibia length(TL,mm)were measured after 4 weeks to assess CH.The pathological changes of myocardial tissue were detected by hematoxylin eosin(HE)staining.The expression levels of miR-208a-3p and GATA4 in myocardial tissue were detected.Dual-luciferase reporter was applied to assess targeting relationships.The effect of over expression of miR-208a-3p on GATA4 expression in cardiomyocytes was detected.Results The level of miR-208a-3p,HW/TL,and myocardial cell surface area in MI group were significantly higher than those in control group,and the levels of GATA4 mRNA and protein were significantly lower than those in control group(P<0.05).The level of miR-208a-3p,HW/TL,and myocardial cell surface area in MI+miR-208a-3p inhibitor group were significantly lower than those in MI group,and the GATA4 mRNA and protein levels were significantly higher than those in MI group(P<0.05).There was targeted binding of miR-208a-3p to GATA4 mRNA in cardiomyocytes.Over expression of miR-208a-3p significantly inhibited the expression of GATA4 mRNA and protein in cardiomyocytes(P<0.05).Conclusions Elevation of miR-208a-3p after MI induces CH through targeted inhibition of GATA4 expression.
维普
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