Role of ubiquitin E3 ligase TRIM10 in regulating cardiomyocyte hyper-trophy
10.3969/j.issn.1000-4718.2017.10.009
- VernacularTitle:泛素E3连接酶TRIM10在心肌细胞肥大中的作用
- Author:
yu Chun ZHOU
1
;
nan Nan LI
;
xia Hong WANG
;
Cui TIAN
;
hua Hui LI
Author Information
1. 首都医科大学基础医学院生理学与病理生理学系
- Keywords:
Ubiquitin E3 ligase;
TRIM10;
Cardiomyocyte hypertrophy
- From:
Chinese Journal of Pathophysiology
2017;33(10):1788-1793
- CountryChina
- Language:Chinese
-
Abstract:
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 .