17beta-Estradiol inhibits vascular smooth muscle cell proliferation and c -fos expression: role of nitric oxide.
- Author:
Dan YANG
1
;
Zhi TAN
;
Jing-Yun PAN
;
Ting-Huai WANG
Author Information
1. Department of physiology, Sun Yat-sen University of Medical Sciences, Guangzhou 510080, thwang@gzsums.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Cell Division;
drug effects;
Cells, Cultured;
Estradiol;
pharmacology;
Female;
Muscle, Smooth, Vascular;
cytology;
metabolism;
Nitric Oxide;
metabolism;
physiology;
Proto-Oncogene Proteins c-fos;
biosynthesis;
RNA, Messenger;
biosynthesis;
Rats;
Rats, Sprague-Dawley
- From:
Acta Physiologica Sinica
2002;54(1):17-22
- CountryChina
- Language:English
-
Abstract:
Rat vascular smooth muscle cells (VSMC) were used to study the effect of 17beta -estradiol (E(2)) on cellular proliferation (cell counting), DNA synthesis ((3)H thymidine incorporation), MTT, c -fos mRNA expression and nitric oxide (NO) release. The results obtained showed that E(2) (10(-12) 10(-8) mol/L) induced NO release from VSMC in a concentration-dependent manner; 10(-8) mol/L E (2)significantly inhibited VSMC cellular proliferation and DNA synthesis induced by 10% FCS and 10(-7) mol/L ET-1, which was obviously reversed by 10(-7)mol/L tamoxifen and 10(-6) mol/L L-NAME; after a pretreatment for 24 hours, 10(-8)mol/L E(2) significantly inhibited VSMC c -fos mRNA expression induced by 10(-7)mol/L ET-1, which was also obviously reversed by 10(-6) mol/L L-NAME. These results suggest that the inhibitory effects of E(2) on VSMC cellular proliferation and c -fos mRNA expression are closely related with NO release in VSMC, which is, at least, partly medicated by ER.
