The effect of 17 beta-estradiol on intracellular calcium homeostasis in human endothelial cells.
The effect of 17 beta-estradiol on intracellular calcium homeostasis in human endothelial cells.
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DOI：
10.1016/j.ejphar.2009.12.030
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发表时间：
2010-03-25
影响因子：
5
通讯作者：
Rahimian R
中科院分区：
文献类型：
--
作者：
Thor D;Uchizono JA;Lin-Cereghino GP;Rahimian R
雌激素对心血管的影响部分是通过增强内皮一氧化氮合酶的功能来介导的。内皮一氧化氮合酶活性取决于许多辅助因子，包括 Ca2+。因此，我们分别使用分光荧光法和蛋白质印迹研究了长期 17 β-雌二醇治疗对人内皮细胞系 EA.hy926 中细胞内 Ca2+ 浓度和内皮一氧化氮合酶蛋白表达的影响。用毒胡萝卜素抑制肌（内）质网 Ca2+ ATP 酶导致细胞内 Ca2+ 浓度增加，与载体处理的细胞相比，长期 17 β-雌二醇处理（1 μM，24 小时）的加载 Fura-2-乙酰氧基甲酯的细胞中的细胞内 Ca2+ 浓度较高，表明 17 β-雌二醇处理的细胞中内质网 Ca2+ 含量较高。在长期 17 β-雌二醇处理的细胞中还观察到 Ca2+ 流入途径增强。此外，与媒介物处理的细胞相比，17 β-雌二醇处理的细胞表达更高水平的内皮一氧化氮合酶蛋白。非选择性雌激素受体抑制剂 ICI 182,780（10 μM， 13-甲基-7-[9-(4,4,5,5,5-五氟戊基亚磺酰基)壬基]-7,8,9,11,12,13,14,15,16,17-十氢-6H-环戊[a]菲-3,17-二醇)。此外，对长期 17 β-雌二醇处理的雌激素受体 α 敲低细胞中毒胡萝卜素诱发的 Ca2+ 反应的分析显示，与媒介物处理的雌激素受体 α 敲低细胞相比，Ca2+ 反应没有显着差异，表明 17 β-雌二醇对 Ca2+ 稳态的调节是通过雌激素受体 α 依赖性途径介导的。这些数据揭示了在 17 β-雌二醇处理的人内皮细胞中，雌激素受体 α 依赖性的 Ca2+ 稳态调节伴随着内皮一氧化氮合酶表达的增强。
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 β-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 β-estradiol-treated (1 μM, 24 h) cells loaded with Fura-2-acetoxymethyl ester compared to vehicle-treated cells, suggesting a higher endoplasmic reticulum Ca2+ content in 17 β-estradiol-treated cells. An enhanced Ca2+ influx pathway in chronically 17 β-estradiol-treated cells was also observed. In addition, 17 β-estradiol-treated cells expressed higher levels of endothelial nitric oxide synthase protein in comparison to vehicle-treated cells. The chronic effect of 17 β-estradiol on Ca2+ homeostasis and endothelial nitric oxide synthase expression was attenuated with the nonselective estrogen receptor inhibitor, ICI 182,780 (10 μM, 13-methyl-7-[9-(4,4,5,5,5-pentafluoropentylsulfinyl)nonyl]-7,8,9,11,12,13,14,15,16,17-decahydro-6H-cyclopenta[a]phenanthrene-3,17-diol). Furthermore, analysis of the thapsigargin-evoked Ca2+ response in chronically 17 β-estradiol-treated estrogen receptor α-knockdown cells showed no significant difference in Ca2+ response compared to vehicle-treated estrogen receptor α-knockdown cells, indicating that the regulation of Ca2+ homeostasis by 17 β-estradiol is mediated through an estrogen receptor α-dependent pathway. These data revealed an estrogen receptor α-dependent modulation of Ca2+ homeostasis accompanying the enhancement of endothelial nitric oxide synthase expression in 17 β-estradiol-treated human endothelial cells.
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影响因子：
4
作者：
Gifford, Shannon M.;Yi, Fu-Xian;Bird, Ian M.
通讯作者：
Bird, Ian M.
DOI：
10.1152/ajplung.1997.273.1.l119
发表时间：
1997-07-01
影响因子：
4.9
作者：
LantinHermoso, RL;Rosenfeld, CR;Shaul, PW
通讯作者：
Shaul, PW
影响因子：
37.8
作者：
REIS, SE;GLOTH, ST;BRINKER, JA
通讯作者：
BRINKER, JA
DOI：
10.1016/j.bbrc.2004.07.137
发表时间：
2004-09-17
影响因子：
3.1
作者：
Rahimian, R;Chan, L;van Breemen, C
通讯作者：
van Breemen, C
DOI：
10.1073/pnas.89.23.11259
发表时间：
1992-12-01
影响因子：
11.1
作者：
HAYASHI, T;FUKUTO, JM;CHAUDHURI, G
通讯作者：
CHAUDHURI, G