17β-Estradiol inhibits cyclic strain-induced endothelin-1 gene expression within vascular endothelial cells.

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 生命科學院 > 生物科技學系暨碩士班 > 期刊論文 > Item 310903500/6232

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题名:	17β-Estradiol inhibits cyclic strain-induced endothelin-1 gene expression within vascular endothelial cells.
作者:	(Juan SH);(Chen JJ);(Chen CH);(Lin H);(Cheng CF);(Liu JC);(Hsieh MH);(Chen YL);(Chao HH);(Chen TH);(Chan P);鄭志鴻(CHENG, TZU-HURNG)*
贡献者:	生命科學院生物科技學系
关键词:	strain;reactive oxygen species;extracellular signal-regulated kinase
日期:	2004-09
上传时间:	2009-08-25 14:39:08 (UTC+8)
摘要:	It has been well documented previously that 17-estradiol (E2) exerts a protective effect on cardiovascular tissue. The possible role of E2 in the regulation of endothelin (ET)-1 production has been previously reported, although the complex mechanisms by which E2 inhibits ET-1 expression are not completely understood. The aims of this study were to examine whether E2 was able to alter strain-induced ET-1 gene expression and also to identify the putative underlying signaling pathways that exist within endothelial cells. For cultured endothelial cells, E2 (1–100 nM), but not 17-estradiol, inhibited the level of strain-induced ET-1 gene expression and also peptide secretion. This inhibitory effect elicited by E2 was able to be prevented by the coincubation of endothelial cells with the estrogen receptor antagonist ICI-182,780 (1 µM). E2 also inhibited strain-enhanced NADPH oxidase activity and intracellular reactive oxygen species (ROS) generation as measured by the redox-sensitive fluorescent dye 2',7'-dichlorofluorescin diacetate and the level of extracellular signal-regulated kinase (ERK) phosphorylation. Furthermore, the presence of E2 and antioxidants such as N-acetylcysteine and diphenylene iodonium were able to elicit a decrease in the level of strain-induced ET-1 secretion, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1 binding activity. In summary, we demonstrated, for the first time, that E2 inhibits strain-induced ET-1 gene expression, partially by interfering with the ERK pathway via the attenuation of strain-induced ROS generation. Thus this study delivers important new insight regarding the molecular pathways that may contribute to the proposed beneficial effects of estrogen on the cardiovascular system.
關聯:	AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY 287(3)H1254 ~H1261
显示于类别:	[生物科技學系暨碩士班] 期刊論文

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