GSNO通过亚硝酰化抑制Myocardin诱导的心肌肥厚  

GSNO Inhibiting Myocardin Induced Cardiomyocyte Hypertrophy Via S-nitrosylation

作　　者：郑德亮 廖兴华[1] 魏兆强 杜福 周浩[1] 张同存[1] ZHENG Deliang;LIAO Xinghua;WEI Zhaoqiang;DU Fu;ZHOU Hao;ZHANG Tongcun(Key Laboratory of Industrial Fermentation Microbiology,Ministry of Education,Tianjin Key Laboratory of Industrial Microbiology College of Biotechnology,Tianjin University of Science & Technology,Tianjin 300457,China)

机构地区：[1]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,天津300457

出　　处：《天津科技大学学报》2017年第4期30-35,共6页Journal of Tianjin University of Science & Technology

基　　金：国家自然科学基金资助项目(31171303)

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.Myocardin can induce cardiomyocyte hupertrophy and nitric oxide can protect cardiac tissue,but the effect of NO on cardiomyocyte hypertrophy remains unclear.First,in this research,NO fluorescent probe was used to detect the level of NO in H9c2cells.The results show that the NO level was significantly increased after S-Nitrosoglutathione(GSNO)treatment.Myocardin could be S-nitrosylated and modified when the cells were treated with200,μmol/L GSNO,and inhibitedα-MHC expression in both mRNA and protein.Finally,overexpressing Myocardin can activate the transcription of GSNO reductase(GSNOR)expression and reduce the amount of intracellular NO.In conclusion,S-nitrosylation can inhibite hypertrophy induced by Myocardin.Myocardin can activate GSNOR transcription and indirectly inhibit GSNO's effect on Myocardin.

关 键 词：亚硝酰化 MYOCARDIN GSNO GSNOR 

分 类 号：Q28[生物学—细胞生物学]