RESUMEN
Objective To investigate the role and possible mechanism of microRNA(miR)144-3p in promoting cardiomyocyte hypertrophy. Methods Forty-five C57BL/ 6 mice were divided into control group, myocardial hypertrophy model group (model group), and miR144-3p transfection group (transfection group) according to their transfection method. The cardiac function related indexes of three groups of mice were detected. HE staining was performed on mouse myocardial tissue.The expression of miR144-3p in mouse cardiomyocytes was detected by Real-time PCR. Antinuclear factor (ANF), β-myosin heavy chain (β-MHC), actin α1 (Acta1) and histone deacetylase 2 (HDAC2) were detected by Western blotting in three groups. Results Compared with the control group, the interventricular septal thickness- diastolic(IVSd), interventricular septal thickness-systolic(IVSs), diastolic left ventricular posterior wall thickness(IVPWd), systolic left ventricular posterior wall thickness(IVPWs), ejection fraction(EF), cardiac weight index and left cardiac index of the model group and the transfection group were significantly higher, while systolic left ventricular diameter (LVDs) and diastolic left ventricular diameter(LVDd)were lower (P0. 05). Compared with the control group, the relative expression of miR144-3p in the model group and the transfection group was significantly higher than that in the model group (P<0. 05). Compared with the control group, the expression levels of antinuclear factor, β-myosin heavy chain, Actinα1 and histone deacetylase 2 in the model group and the transfected group were significantly higher (P<0. 05). Conclusion miR144-3p can aggravate cardiac hypertrophy by up-regulating HDAC2 and is expected to become a new therapeutic target.