The inhibitory effect of trilinolein on norepinephrine-induced beta-myosin heavy chain promoter activity, reactive oxygen species generation, and extracellular signal-regulated kinase phosphorylation in neonatal rat cardiomyocytes

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题名:	The inhibitory effect of trilinolein on norepinephrine-induced beta-myosin heavy chain promoter activity, reactive oxygen species generation, and extracellular signal-regulated kinase phosphorylation in neonatal rat cardiomyocytes
作者:	Liu, JC;Chan, P;Chen, JJ;Lee, HM;Lee, WS;Shih, NL;Chen, YL;Hong, HJ;Cheng, TH
贡献者:	中醫學院中醫系;Taipei Med Univ, Wan Fang Hosp, Dept Med, Taipei 117, Taiwan;Taipei Med Univ, Wan Fang Hosp, Grad Inst Med Sci, Taipei 117, Taiwan;Taipei Med Univ, Wan Fang Hosp, Grad Inst Biomed Technol, Taipei 117, Taiwan;Acad Sinica, Inst Biomed Sci, Taipei 115, Taiwan;Natl Taiwan Univ Hosp, Dept Internal Med, Taipei 100, Taiwan;Natl Taiwan Univ, Coll Med, Taipei, Taiwan;Natl Def Med Ctr, Dept Pharmacol, Taipei, Taiwan;China Med Coll, Sch Chinese Med, Taichung, Taiwan
日期:	2004
上传时间:	2010-09-24 13:41:53 (UTC+8)
出版者:	KARGER
摘要:	It is well documented that 17beta-estradiol (E-2) exerts a cardiovascular protective effect. A possible role of E-2 in the regulation of endothelin-1 ( ET-1) production has been reported. However, the complex mechanisms by which E-2 inhibits ET-1 expression are not completely understood. The aims of this study were to examine whether E-2 may alter angiotensin II (Ang II)-induced cell proliferation and ET-1 gene expression and to identify the putative underlying signaling pathways in rat aortic smooth muscle cells. Cultured rat aortic smooth muscle cells were preincubated with E-2, then stimulated with Ang II, and [H-3] thymidine incorporation and ET-1 gene expression were examined. The effect of E-2 on Ang-II-induced extracellular signal-regulated kinase (ERK) phosphorylation was tested to elucidate the intracellular mechanism of E-2 in proliferation and ET-1 gene expression. Ang II increased DNA synthesis which was inhibited with E-2 ( 1 - 100 nM). E-2, but not 17alpha-estradiol, inhibited the Ang-II-induced ET-1 gene expression as revealed by Northern blotting and promoter activity assay. This effect was prevented by coincubation with the estrogen receptor antagonist ICI 182,780 (1 muM). E-2 also inhibited Ang-II-increased intracellular reactive oxygen species (ROS) as measured by a redox-sensitive fluorescent dye, 2', 7'-dichlorofluorescin diacetate, and ERK phosphorylation. Furthermore, E-2 and antioxidants, such as N-acetyl cysteine and diphenylene iodonium, decreased Ang-II-induced cell proliferation, ET-1 promoter activity, ET-1 mRNA, ERK phosphorylation, and activator protein-1-mediated reporter activity. In summary, our results suggest that E-2 inhibits Ang-II-induced cell proliferation and ET-1 gene expression, partially by interfering with the ERK pathway via attenuation of ROS generation. Thus, this study provides important new insight regarding the molecular pathways that may contribute to the proposed beneficial effects of estrogen on the cardiovascular system. Copyright (C) 2004 National Science Council, ROC and S. Karger AG, Basel.
關聯:	JOURNAL OF BIOMEDICAL SCIENCE 11(1):11-18
显示于类别:	[中醫學系暨碩博班] 期刊論文

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