Angiotensin II type 1 receptor is required for the cardiac fibrosis triggered by mechanical stress independent of Ang II in mice
- Author:
Yong YE
;
Hui GONG
;
Jian WU
;
Zhiwen DING
;
Yi SHEN
;
Peipei YIN
;
Xingxu WANG
;
Jieyun YOU
;
Shijun WANG
;
Jie YUAN
;
Guoliang JIANG
;
Jiayuan HUANG
;
Weijing ZHANG
;
Junbo GE
;
Yunzeng ZOU
- Publication Type:Journal Article
- From:
Chinese Journal of Pathophysiology
2016;32(8):1500-1500
- CountryChina
- Language:Chinese
-
Abstract:
AIM:We investigated how AT 1-R stimulated by mechanical stresses induces cardiac fibrosis .METHODS:We produced in vivo cardiac pressure overload model in angiotensinogen knockout ( ATG-/-) mice and in vitro mechanically-stretched cell model in cultured neonatal cardiac cells of ATG-/-mice both lack the participation of Ang II .RESULTS: Pressure overload for 4 weeks in ATG-/-mice induced myocardial hypertrophy accompanied by the significant interstitial fibrosis , however , the TGF-β, a key regulatory factor of fibrosis, was not significantly increased in these ATG-/-mice.Meanwhile, the inhibitor for AT1-R significantly inhibited mechani-cal stress-induced cardiac fibrosis in these ATG-/-models whereas inhibition of TGF-βdid not.CONCLUSION:The results showed that mechanical stress-induced fibrotic responses through AT 1-R required the phosphorylation of Smad 2 but not the involvement of TGF-β.
