17beta-Estradiol inhibits vascular smooth muscle cell proliferation and c -fos expression: role of nitric oxide.
Dan Yang, Zhi Yong Tan, Jing-Yun Pan, Tinghuai Wang
Abstract
Dan Yang, Zhi Yong Tan, Jing-Yun Pan, Tinghuai Wang
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.
OpenAlex reports 5 citations for this work. Citation counts describe recorded attention and do not establish research quality.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
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.
Key concepts: Vascular smooth muscle, DNA synthesis, Nitric oxide, Cell growth, Messenger RNA, Mole, Endocrinology, Molecular biology