Angiotensin II induces endothelin-1 Gene expression via Reactive Oxygen Species-sensitive Extracellular Signal-regulated Kinase Pathway in Rat Aortic

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题名:	Angiotensin II induces endothelin-1 Gene expression via Reactive Oxygen Species-sensitive Extracellular Signal-regulated Kinase Pathway in Rat Aortic
作者:	洪宏杰(Hong,Hong-Jye)
贡献者:	中醫學院中醫學系學士班中醫基礎學科
日期:	2003-10-30
上传时间:	2009-09-03 16:04:35 (UTC+8)
摘要:	Angiotensin II induces Endothelin-1 Gene Expression via Reactive Oxygen Species–sensitive Extracellular Signal-regulated Kinase Pathway in Rat Aortic Smooth Muscle Cells. Hong-Jye Honga, Tzu-Hurng Chengb aSchool of Chinese Medicine, China Medical College, Taichung, Taiwan, R.O.C. bDepartment of Medicine and Clinical Research Center, Taipei Medical University-Wan Fang Hospital, Taipei, Taiwan, R.O.C. e-mail: [email protected] Tel:886-2-22053366ext 1603 Fax:886-2-22013703 Preferred presentation style: poster ABSTRACT Background: Angiotensin II (Ang II) increases vascular endothelin-1 (ET-1) tissue levels, which in turn mediate a major part of Ang II–stimulated vascular growth and hypertension in vivo. Ang II also stimulates reactive oxygen species (ROS) generation in vascular smooth muscle cells. However, whether ROS are involved in Ang II-induced ET-1 gene expression in vascular smooth muscle cells remains to be determined. Methods: Cultured rat aortic smooth muscle cells were stimulated with Ang II, [3H]thymidine incorporation and the ET-1 gene expression were examined. Antioxidant pretreatment on Ang II-induced extracellular signal-regulated kinase (ERK) phosphorylation were performed to elucidate the redox-sensitive pathway in proliferation and ET-1 gene expression. Results: Ang II increased DNA synthesis which was inhibited with both AT1 receptor antagonist (olmesartan) and ETA receptor antagonist (BQ485). ET-1 gene was induced with Ang II as revealed by Northern blotting and promoter activity assay. Ang II-increased intracellular ROS levels were inhibited by olmesartan and antioxidants. Antioxidants suppressed Ang II-induced ET-1 gene expression. Ang II-activated ERK phosphorylation was also significantly inhibited by antioxidants. An ERK inhibitor U0126 fully inhibited Ang II-induced ET-1 expression. Truncation and mutational analysis of the ET-1 gene promoter showed that activator protein-1 (AP-1) binding site was an important cis-element in
關聯:	The 26Annual Scientific Meeting of the Japanese Society of Hyper
显示于类别:	[中醫學系暨碩博班] 會議論文

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