泛素E3连接酶TRIM10在心肌细胞肥大中的作用  

Role of ubiquitin E3 ligase TRIM10 in regulating cardiomyocyte hypertrophy

作　　者：周春宇[1] 李南南[1] 王红霞[1] 田翠[1] 李汇华[1] 

机构地区：[1]首都医科大学基础医学院生理学与病理生理学系,北京100069

出　　处：《中国病理生理杂志》2017年第10期1788-1793,共6页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金重点项目(No.81330003)

摘　　要：目的:探讨泛素E3连接酶TRIM10在心肌细胞肥大中的作用及分子机制。方法:培养原代的大鼠乳鼠心肌细胞,siRNA-TRIM10与siRNA对照(siRNA-control)或过表达腺病毒Ad-TRIM10与空载对照Ad-GFP转染细胞24 h,然后用苯肾上腺素(phenylephrine,PE)处理细胞24 h。Western blot检测TRIM10、AKT和ERK1/2的蛋白水平;免疫荧光染色观察心肌细胞的大小;实时荧光定量PCR检测心房钠尿肽(ANP)和脑钠尿肽(BNP)的mRNA的表达水平。结果:与对照组相比,PE处理明显上调心肌细胞中TRIM10蛋白的表达水平。siRNA-TRIM10敲低内源性TRIM10表达后明显减小PE诱导的心肌细胞体积,抑制ANP和BNP的mRNA的表达以及降低AKT和ERK1/2的磷酸化水平;而过表达TRIM10则呈现出与siRNA-TRIM10完全相反的结果。结论:TRIM10可调节心肌细胞肥大,其作用可能与AKT和ERK信号相关。AIM：To explore the role of ubiquitin E3 ligase tripartite motif 10 （TRIM10） in the development of cardiomyocyte hypertrophy .METHODS： Primary cultured neonatal rat cardiomyocytes （ NRCMs ） were infected with siRNA-TRIM10, siRNA-control, Ad-TRIM10 or Ad-GFP for 24 h respectively, and then stimulated with phenylephrine （ PE） for additional 24 h.The protein levels of TRIM10, AKT and ERK1/2 were determined by Western blot .The size of the NRCMs was measured by immunofluorescence staining .The mRNA expression of atrial natriuretic peptide （ ANP） and brain natriuretic peptide （ BNP） was detected by RT-qPCR.RESULTS：Compared with the control , PE treatment signifi-cantly increased the protein expression of TRIM 10.Moreover, transfection of NRCMs with siRNA-TRIM10 markedly inhibi-ted cardiomyocyte size , the mRNA expression of ANP and BNP , and the phosphorylation levels of AKT and ERK as com-pared with siRNA-control after PE treatment.In contrast, overexpression of TRIM10 significantly enhanced PE-induced hy-pertrophic effect on NRCMs above .CONCLUSION：TRIM10 regulates cardiomyocyte hypertrophy partially through AKT and ERK signaling pathways .

关 键 词：泛素E3连接酶 TRIM10 心肌细胞肥大 

分 类 号：R54[医药卫生—心血管疾病] R363[医药卫生—内科学]