[Possible involvement of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells by 17beta-estradiol].
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.
Tan
Zhi
Z
Department of Physiology, College of Basic Medical Sciences, Sun Yat-Sen University, Guangzhou 510089, China.
Lin
Gui-Ping
GP
Wang
Ting-Huai
TH
D000818:Animals; D001013:Aorta, Thoracic / Q000166:cytology; D051242:Caveolin 1 / Q000502:physiology*; D002455:Cell Division; D002478:Cells, Cultured; D019332:Endothelin-1 / Q000037:antagonists & inhibitors / Q000502:physiology*; D004958:Estradiol / Q000494:pharmacology*; D009131:Muscle, Smooth, Vascular / Q000166:cytology*; D051381:Rats; D017207:Rats, Sprague-Dawley
D051242:Caveolin 1; D019332:Endothelin-1; D004958:Estradiol