Possible involvement of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells by 17beta-estradiol.
- Author:
Zhi TAN
1
;
Gui-Ping LIN
;
Ting-Huai WANG
Author Information
1. Department of Physiology, College of Basic Medical Sciences, Sun Yat-Sen University, Guangzhou 510089, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta, Thoracic;
cytology;
Caveolin 1;
physiology;
Cell Division;
Cells, Cultured;
Endothelin-1;
antagonists & inhibitors;
physiology;
Estradiol;
pharmacology;
Muscle, Smooth, Vascular;
cytology;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2004;56(3):379-383
- CountryChina
- Language:Chinese
-
Abstract:
The aim of the present study was to investigate the role of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells (VSMCs) by 17beta-estradiol. In the cultured rat thoracic aortic VSMCs, proliferation of VSMCs was determined by using [(3)H]-thymidine incorporation and the expression of caveolin-1 protein was measured by immunofluorescence assays and Western blotting. The measurement demonstate VSMCs exposed to various concentrations of endothelin-1 (1-100 nmol/L) for 24 h induced an increase in [(3)H]-thymidine incorporation. Pretreament with various concentrations of 17beta-estradiol (0.1-10 nmol/L) for 24 h inhibited the proliferation effect of endothelin-1. Immunofluorescence assays showed that after 24 h treatment of VSMCs with endothelin-1 (100 nmol/L), the expression of caveolin-1 in VSMCs was significantly increased, whereas pretreament with 17beta-estradiol (10 nmol/L) for 24 h inhibited the effect. Western blotting results further proved that endothelin-1 inhibited and 17beta-estradiol increased the expression of caveolin-1 in VSMCs. These results demonstrate that 17beta-estradiol inhibits the VSMCs proliferation induced by endothelin-1, and that the effect of estradiol is probably mediated by caveolin-1.
