RhoE Improves Ang Ⅱ-Induced Myocardial Fibrosis by Inhibiting Activation of Smad3 Signaling Pathway
10.11969/j.issn.1673-548X.2025.04.010
- VernacularTitle:RhoE通过抑制Smad3信号通路的激活改善Ang Ⅱ诱导的心肌纤维化
- Author:
Penghua YOU
1
;
Xiaomin HE
;
Bixue ZHANG
Author Information
1. 710068 西安,陕西省人民医院心血管内科
- Publication Type:Journal Article
- Keywords:
Angiotensin Ⅱ;
Ventricular remodeling;
Myocardial fibrosis;
RhoE
- From:
Journal of Medical Research
2025;54(4):45-51
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the protective effect and mechanism of RhoE overexpression in angiotensin Ⅱ-induced myo-cardial fibrosis.Methods Primary cardiomyocytes were cultured in vitro using angiotensin Ⅱ-induced myocardial fibrosis model,and transfected with M-RhoE-carrying overexpressing adenovirus and overexpressing RhoE according to subgroup.α-SMA and Smad3 ex-pression distribution in primary cardiomyocytes were detected by immunofluorescence.The protein expression levels of RhoE,GAPDH,α-SMA,Smad3 and p-Smad3 in primary cells were detected by Western blotting.Results Ang Ⅱ interferes with primary cardiomyo-cytes.Western-blot analysis showed that compared with the control group,the expression levels of p-Smad3 and α-SMA in Ang Ⅱgroup were increased,while the expression levels of RhoE were decreased(P＜0.05).After transfection of RhoE overexpressing adenovi-rus,Western blot results showed that the α-SMA expression level in Ang Ⅱ group was increased compared with that in the control group(P＜0.05).Compared with Ang Ⅱ group α-SMA expression level in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence detection showed that the α-SMA fluorescence intensity in Ang Ⅱ group was increased compared with that in control group(P＜0.05).Compared with Ang Ⅱ group α-SMA fluorescence intensity in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Effects of overexpression of RhoE gene on TGF-β1/Smad3 pathway.Western blot results showed that compared with the control group,the p-Smad3/Smad3 ratio in Ang Ⅱ group was increased(P＜0.05).Compared with Ang Ⅱ group,the p-Smad3/Smad3 ratio in Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Immunofluorescence nuclear translocation showed that compared with the control group,the red fluorescence in myocardial nucleus of Ang Ⅱ group was significantly increased(P＜0.05).Compared with Ang Ⅱ group,the red fluorescence in myocardial nucleus of Ang Ⅱ+Ad-RhoE group was significantly decreased(P＜0.05).Conclusion The process of Ang Ⅱ-induced myocardial fibrosis is accompanied by the activation of TGF-β1/Smad3 sig-naling pathway,and RhoE can inhibit Ang Ⅱ-induced myocardial fibrosis by inhibiting TGF-β1/Smad3 signaling pathway.
