miR-455-3p通过靶基因HDAC2抑制心肌梗死后心肌肥厚

miR-455-3p inhibits cardiac hypertrophy in mice with myocardial infarction by targeting HDAC2

目的:探讨miR-455-3p在心肌梗死后心肌肥厚中的作用。方法:比较miR-455-3p在心肌梗死组和空白对照组的表达。心肌细胞过表达miR-455-3p情况下分析细胞表面积和心肌肥厚基因表达。荧光素酶活性检测和Western blot法确定受miR-455-3p调控的靶基因。通过心肌梗死模型组大鼠体内miR-455-3p的过表达确定miR-455-3p对心肌肥厚的影响。结果:在体外和体内试验中发现在心肌肥厚中miR-455-3p均被下调。体外实验,过度表达miR-455-3p可以抑制心肌肥厚。与miR-455-3p相比,心肌肥厚中HDAC2被上调。HDAC2是一种新型的miR-455-3p靶基因。心肌梗死大鼠过表达miR-455-3p通过降低HDAC2的表达能抑制心肌梗死后心肌肥厚。结论:miR-455-3p是心肌肥厚的重要调节因子,为心肌梗死后心肌肥厚的治疗提供新的理论基础。

Objective To evaluate the role of miR-455-3p in cardiac hypertrophy after Myocardial in faretion （MI）. Methods The expression of miR-455-3p was tested in sham-operation and post-MI group. The cell surface area and the cardiac hypertrophy gene expression were analyzed in primary cardiomyocytes with miR- 455-3p overexpression. In addition, luciferase assay and western blot were used for determining the target gene expression regulated by miR-455-3p. Finallyly, the regulating effect of miR-455-3p on cardiac hypertrophy was determined by in vivo overexpression of miR-455-3p in MI surgery group. Results oth in vitro and in vivo miR- 455-3p were down-regulated in cardiac hypertrophy, in vitro overexpression of miR-455-3p inhibited cardiomyocytes hypertrophy. In contrast to miR-455-3p expression, HDAC2 was up-regulated during cardiac hypertrophy. The in vivo overexpression of miR-455-3p effectively attenuated myocardial infarction-induced cardiac hypertrophy by way of inhibiting the expression of HDAC2. Conclusions miR-455-3p may be a key regulator to cardiac hy pertrophy, thus offering a new therapeutic strategy for myocardial infarction-induced cardiac hypertrophy.