The effect of 17 β-estradiol on intracellular calcium homeostasis in human endothelial cells

被引：12
作者：
Thor, Der [1 ]
Uchizono, James A. [2 ]
Lin-Cereghino, Geoff P. [3 ]
Rahimian, Roshanak [1 ]
机构：
[1] Univ Pacific, Thomas J Long Sch Pharm & Hlth Sci, Dept Physiol & Pharmacol, Stockton, CA 95211 USA
[2] Univ Pacific, Thomas J Long Sch Pharm & Hlth Sci, Dept Pharmaceut & Med Chem, Stockton, CA 95211 USA
[3] Univ Pacific, Dept Biol Sci, Stockton, CA 95211 USA
来源：
EUROPEAN JOURNAL OF PHARMACOLOGY | 2010年 / 630卷 / 1-3期
关键词：
Estrogen; Estrogen receptor alpha; Endothelial nitric oxide synthase; Calcium; NITRIC-OXIDE SYNTHASE; CORONARY-HEART-DISEASE; ESTROGEN-RECEPTOR; POSTMENOPAUSAL WOMEN; HORMONE-THERAPY; CA2+ ENTRY; RAT AORTA; RELEASE; REPLACEMENT; ATHEROSCLEROSIS;
D O I：
10.1016/j.ejphar.2009.12.030
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
The cardiovascular effects of estrogen are mediated in part by augmenting the function of endothelial nitric oxide synthase Endothelial nitric oxide synthase activity is dependent on many cofactors including Ca2+ Hence, we investigated the effect of chronic 17 beta-estradiol treatment on the intracellular Ca2+ concentration and endothelial nitric oxide synthase protein expression in the human endothelial cell line, EA.hy926. using spectrofluorometry and Western blot, respectively Inhibiting the sarco(endo)plasmic reticulum Ca2+ ATPase with thapsigargin caused an increase in the intracellular Ca2+ concentration, which was higher in chronically 17 beta-estradiol-treated (1 mu M, 24 h) cells loaded with Fura-2-acetoxymethyl ester compared to vehicle-treated cells, suggesting a higher endoplasmic reticulum Ca2+ content in 17 beta-estradiol-treated cells. An enhanced Ca2- Influx pathway in chronically 17 beta-estradiol-treated cells was also observed In addition. 17 beta-estradiol-treated cells expressed higher levels of endothelial nitric oxide synthase protein in comparison to vehicle-treated cells The chronic effect of 17 beta-estradiol on Ca2+ homeostasis and endothelial nitric oxide synthase expression was attenuated with the nonselective estrogen receptor inhibitor, 10 182,780 (10 mu M, 7 alpha, 17 beta-[9-[(4,4,5,5,5-Pentafluoropentyl)sulfinyl]nonyl] estra-1,3,5(10)-triene-3,17-diol). Furthermore. analysis of the thapsigargin-evoked Ca2+ response in chronically 17 beta-estradiol-treated estrogen receptor alpha-knockdown cells showed no significant difference in Ca2+ response compared to vehicle-treated estrogen receptor alpha-knockdown cells, indicating that the regulation of Ca2+ homeostasis by 17 beta-estradiol is mediated through an estrogen receptor alpha-dependent pathway These data revealed an estrogen receptor alpha-dependent modulation of Ca2+ homeostasis accompanying the enhancement of endothelial nitric oxide synthase expression in 17 beta-estradiol-treated human endothelial cells. (C) 2009 Elsevier B V All rights reserved
引用
收藏
页码：92 / 99
页数：8
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