The effects of 17?-estradiol on cardiomyocyte hypertrophy induced by endothelin
- VernacularTitle:雌激素对内皮素诱导心肌细胞肥大反应的影响及其机制
- Author:
Yimin GUO
;
Hong PAN
;
Yuhong CUI
;
Guiping LIN
;
Tinghuai WANG
- Publication Type:Journal Article
- Keywords:
Estradiol;
Myocardial hypertrophy;
Endothelin-1;
Extracellular signal-regulated kinases
- From:
Chinese Journal of Pathophysiology
2000;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the effect of 17?-estradiol(E2) on myocardial hypertrophy induced by endothelin-1(ET-1) and the related mechanism.METHODS: Myocardial cells from neonate rats were cultured in vitro and myocardial hypertrophy model was established with ET-1.The effects of 17?-estradiol on myocardial hypertrophy were observed.The role of ERK1/2 in the effects of 17?-estradiol was also detected.RESULTS: Compared with control group,ET-1 increased cell protein content,cell surface area and -Leucine(-Leu) incorporation.Pretreatment with E2 for 24 h could inhibit the increase in cell protein content,cell surface area and -Leu incorporation induced by ET-1.ET-1 significantly stimulated ERK1/2 activity,which was prevented by pretreatment with E2.Tamoxifen,estradiol receptor antagonist,partially inhibited the effect of E2.The ability of ET-1 to stimulate -Leu incorporation was significantly blocked by PD98059,which could enhance the inhibitory effect of E2 on the increase of -Leu incorporation in cardiomyocytes induced by ET-1.CONCLUSION: E2 can inhibit cardiomyocyte hypertrophy induced by ET-1.This effect is mediated by estrogen receptor.ERK1/2 signal pathway is closely correlated with the inhibitory effect of E2 on cardiomyocyte hypertrophy induced by ET-1.
