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Effect of ERK on 17#beta#-estradiol-induced inhibition of VSMC proliferation in rats after vascular injury

Wang Tinghuai, Tan Zhi, Fu Xiaodong, Yang Dan, Hu Feixue, Li Yongyong

Department of Physiology,Zhongshan Medical College of Sun Yat-Sen Univrsity.Guangzhou 510080,Guangdong

Abstract

The results showed that compared with OVX, the vessel wall was signifiantly thickened and the plasma content of NO was signficantly decreased in OVX+Inj group, E_(2) significantly decreased the vessel thickness but increased the plasma NO content after balloon injury. E_(2) inhibited the expression of ERK, phosphorylated ERK and induced the eNOS expression. There is a positive correlation between plasma NO content and eNOS protein expression, while there is a negative correlation between plasma NO content and the thickness of vessel. The plasma NO content and the expression of ERK protein were negatively correlated. These results suggest that E_(2) increases the vascular eNOS protein expression and NO release, leading to the inhibition of VSMC proliferation after balloon injury by inhibiting the ERK and phosphorylated ERK protein expression.

Key words: Extracellular signal-regulated kinase;17#beta#-estradiol;Nitric oxide vascular;Smooth muscle cells

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Citing This Article：

Wang Tinghuai, Tan Zhi, Fu Xiaodong, Yang Dan, Hu Feixue, Li Yongyong. Effect of ERK on 17#beta#-estradiol-induced inhibition of VSMC proliferation in rats after vascular injury. Acta Physiol Sin 2003; 55 (4): (in Chinese with English abstract).