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GSNO通过亚硝酰化抑制Myocardin诱导的心肌肥厚

发布时间:2018-08-28 15:16
【摘要】:Myocardin可以诱导心肌肥厚,而一氧化氮(NO)对于心肌具有一定保护作用,但在心肌肥厚发生的过程中,NO的作用尚未报道.本文首先用NO荧光探针检测亚硝基谷胱甘肽(S-Nitrosoglutathione,GSNO)处理能够引起H9c2细胞中NO总含量的上升.随后利用200,μmol/L GSNO处理细胞,检测发现Myocardin可以发生亚硝酰化修饰,同时心肌肥厚标志基因α-MHC在mRNA水平和蛋白水平的表达均下调.最后通过荧光素酶报告分析、RT-PCR以及Western blot分析表明,过表达Myocardin可以激活GSNO还原酶(GSNO reductase,GSNOR)的表达,并且降低细胞内NO总量.以上结果表明,亚硝酰化可以抑制由Myocardin诱导的心肌肥厚的发生,同时Myocardin可以激活GSNOR的转录,间接抑制GSNO对Myocardin的作用.
[Abstract]:Myocardin can induce myocardial hypertrophy, but nitric oxide (NO) has a protective effect on myocardium, but the role of no in the process of myocardial hypertrophy has not been reported. In this paper, NO fluorescence probe was used to detect that S-Nitrosoglutathione glutathione (GSNO) treatment could increase the total NO content in H9c2 cells. After treated with 200 渭 mol/L GSNO, it was found that Myocardin could be modified by nitrite, and the expression of 伪 -MHC, a marker of myocardial hypertrophy, was down-regulated at the level of mRNA and protein. Finally, RT-PCR and Western blot analysis showed that overexpression of Myocardin could activate the expression of GSNO reductase (GSNO reductase,GSNOR) and decrease the total amount of NO in cells. These results suggest that nitrite can inhibit the occurrence of myocardial hypertrophy induced by Myocardin and that Myocardin can activate the transcription of GSNOR and indirectly inhibit the effect of GSNO on Myocardin.
【作者单位】: 工业发酵微生物教育部重点实验室天津市工业微生物重点实验室天津科技大学生物工程学院;
【基金】:国家自然科学基金资助项目(31171303)
【分类号】:R542.2


本文编号:2209777

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