Interaction of PKC? and Raf in the activation of ERK1/2 in rat vascular smooth muscle cells induced by Ang Ⅱ
- VernacularTitle:PKC?与Raf在AngⅡ引起的大鼠血管平滑肌细胞ERK1/2活化中的作用
- Author:
Yali ZHAO
;
Zhiguo ZHANG
;
Jie LIU
;
Li LI
;
Limei LIU
;
Liling WU
- Publication Type:Journal Article
- Keywords:
Vascular smooth muscle cells;
Protein kinase C;
Angiotensin Ⅱ;
Signal transduction
- From:
Chinese Journal of Pathophysiology
1986;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the crosstalk of PKC? isoform with Raf in the signal pathway of vascular smooth muscle cell(VSMC)hypertrophy induced by angiotensin II(Ang Ⅱ).METHODS:The protein synthesis of VSMCs was measured by [3H]-thymidine incorporation.The expression of PKC? and ERK1/2 proteins were detected by Western blotting.The interaction of the signal molecules was examined by immunoprecipitation.RESULTS:Pretreatment of VSMCs with PKC non-specific inhibitor staurosporine or PKC? pseudosubstrate inhibitor(PS-PKC?),the Ang Ⅱ-induced [3H]-thymidine incorporation into VSMCs was decreased markedly.PS-PKC? pretreatment significantly decreased phosphorylation of ERK1/2 induced by Ang Ⅱ.Compared with VSMCs transfected with wild type Raf,PKC? phosphorylation was similar in the VSMCs transfected with dominant negative Raf(Raf S621A).Immunoprecipitation analysis showed that Ang Ⅱ stimulated the association of Ras with Raf,but PKC? inhibitor had no influence on Ang Ⅱ-induced conjugation of Ras with Raf.After Raf activity was inhibited by Raf S621A,Ang Ⅱ-induced ERK1/2 phosphorylation level declined.CONCLUSION:These results suggest that PKC? is involved in protein synthese induced by Ang Ⅱ in VSMCs,but PKC? induces ERK1/2 activation via a Raf-independent pathway.
