Effect of ERK on 17beta-estradiol-induced inhibition of VSMC proliferation in rats after vascular injury.
- Author:
Ting-Huai WANG
1
;
Zhi TAN
;
Xiao-Dong FU
;
Dan YANG
;
Fei-Xue HU
;
Yong-Yong LI
Author Information
1. Department of Physiology, Zhongshan Medical College of Sun Yat Sen University, Guangzhou 510080. thwang@gzsums.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Carotid Artery, Common;
pathology;
Catheterization;
adverse effects;
Cell Proliferation;
drug effects;
Estradiol;
pharmacology;
Extracellular Signal-Regulated MAP Kinases;
physiology;
Female;
Muscle, Smooth, Vascular;
cytology;
Myocytes, Smooth Muscle;
cytology;
drug effects;
physiology;
Nitric Oxide;
blood;
Nitric Oxide Synthase Type III;
metabolism;
Ovariectomy;
Phosphorylation;
Rats
- From:
Acta Physiologica Sinica
2003;55(4):411-416
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the effect of ERK on 17beta-estradiol (E(2)) inhibition of vascular smooth muscle cell (VSMC) proliferation in rats after vascular injury. Common carotid artery balloon-injury (Inj) model was established in ovariectomized rats (OVX). Female SD rats were randomly divided into 4 groups: OVX, E(2)+OVX, OVX+Inj, and E(2)+OVX+Inj groups. The thickness of the vessels, the plasma content of NO, and the expression of ERK, phosphorylated ERK as well as eNOS protein were measured. The results showed that compared with OVX, the vessel wall was significantly thickened and the plasma content of NO was significantly 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.
