miR-455-3p通过靶基因HDAC2抑制心肌梗死后心肌肥厚

发布时间：2018-05-06 16:37

  本文选题：心肌梗死 + miR--p　； 参考：《实用医学杂志》2016年22期

【摘要】：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。
[Abstract]:Objective: to investigate the role of miR-455-3p in myocardial hypertrophy after myocardial infarction. Methods: to compare the expression of miR-455-3p in myocardial infarction group and blank control group. Cell surface area and myocardial hypertrophy gene expression were analyzed when myocardial cells were overexpressed by miR-455-3p. Luciferase activity and Western blot assay were used to identify target genes regulated by miR-455-3p. The effect of miR-455-3p on myocardial hypertrophy was determined by overexpression of miR-455-3p in myocardial infarction model group. Results: miR-455-3p was down-regulated in myocardial hypertrophy in vitro and in vivo. In vitro, overexpression of miR-455-3p can inhibit myocardial hypertrophy. Compared with miR-455-3p, HDAC2 is up-regulated in myocardial hypertrophy. HDAC2 is a novel miR-455-3p target gene. Overexpression of miR-455-3p can inhibit myocardial hypertrophy after myocardial infarction by decreasing the expression of HDAC2. Conclusion the ratio miR-455-3p is an important regulatory factor for myocardial hypertrophy, which provides a new theoretical basis for the treatment of myocardial hypertrophy after myocardial infarction.
【作者单位】： 郑州大学第二附属医院心内科;郑州大学第二附属医院干部病房;
【基金】：河南省科技攻关计划项目(编号:142102310109) 河南省高等学校重点科研项目(编号:15A320019)
【分类号】：R542.22
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本文编号：1853053