北京大学医学部机构知识库
Advanced  
IR@PKUHSC  > 基础医学院  > 心血管所  > 期刊论文
学科主题: 基础医学
题名:
Angiotensin II up-regulates soluble epoxide hydrolase in vascular endothelium in vitro and in vivo
作者: Ai, Ding; Fu, Yi; Guo, Deliang; Tanaka, Hiromasa; Wang, Nanping; Tang, Chaoshu; Hammock, Bruce D.; Shyy, John Y. -J.; Zhu, Yi
关键词: endothelial cells ; arachidonic acid ; AP-1 ; promoter ; hypertension
刊名: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
发表日期: 2007-05-22
DOI: 10.1073/pnas.0703229104
卷: 104, 期:21, 页:9018-9023
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Multidisciplinary Sciences
研究领域[WOS]: Science & Technology - Other Topics
关键词[WOS]: EPOXYGENASE-DERIVED EICOSANOIDS ; SMOOTH-MUSCLE-CELLS ; KAPPA-B KINASE ; EPOXYEICOSATRIENOIC ACIDS ; ACTIVATOR PROTEIN-1 ; GENE-EXPRESSION ; HYPERTENSION ; PHOSPHORYLATION ; PATHWAYS ; P65
英文摘要:

Epoxyeicosatrienoic acids (EETs), as metabolites of arachidonic acid, may function as antihypertensive and antiatherosclerotic mediators for vasculature. EETs are degraded by soluble epoxide hydrolase (sEH). Pharmacological inhibition and genetic ablation of sEH have been shown to increase the level of EETs, and treating angiotensin II (Ang II)-infused hypertension rats with sEH-selective inhibitors increased the levels of EETs with attendant decrease in systolic blood pressure. To elucidate the mechanisms by which Ang II regulates sEH expression, we treated human umbilical vein endothelial cells (ECs) and bovine aortic ECs with Ang II and found increased sEH expression at both the mRNA and protein levels. Transient transfection assays showed that the activity of the human sEH promoter was increased in ECs in response to Ang II. Further analysis of the promoter region of the sEH gene demonstrated that treatment with Ang II, like overexpression of c-Jun/c-Fos, activates the sEH promoter through an AP-1-binding motif. The binding of c-Jun to the AP-1 site of the sEH promoter was confirmed by chromatin immunoprecipitation assays. in contrast, adenovirus overexpression of the dominant-negative mutant of c-Jun significantly attenuated the effects of Ang II on sEH induction. An elevated level of sEH was found in the aortic intima of both spontaneously hypertensive rats and Ang II-infused Wistar rats. Blocking Ang II binding to Ang II receptor 1 by losartan abolished the sEH induction. Thus, AP-1 activation is involved in the transcriptional up-regulation of sEH by Ang II in ECs, which may contribute to Ang II-induced hypertension.

语种: 英语
WOS记录号: WOS:000246853700061
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67797
Appears in Collections:基础医学院_心血管所_期刊论文

Files in This Item:
File Name/ File Size Content Type Version Access License
PNAS-2007-Ai-9018-23.pdf(1456KB)期刊论文作者接受稿限制开放 联系获取全文

作者单位: 1.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Key Lab Mol Cardiovasc Sci,Educ Minist, Beijing 100083, Peoples R China
2.Peking Univ, Cardiovasc Res Inst, Beijing 100083, Peoples R China
3.Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA
4.Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA
5.Univ Calif Davis, Canc Res Ctr, Davis, CA 95616 USA

Recommended Citation:
Ai, Ding,Fu, Yi,Guo, Deliang,et al. Angiotensin II up-regulates soluble epoxide hydrolase in vascular endothelium in vitro and in vivo[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,2007,104(21):9018-9023.
Service
Recommend this item
Sava as my favorate item
Show this item's statistics
Export Endnote File
Google Scholar
Similar articles in Google Scholar
[Ai, Ding]'s Articles
[Fu, Yi]'s Articles
[Guo, Deliang]'s Articles
CSDL cross search
Similar articles in CSDL Cross Search
[Ai, Ding]‘s Articles
[Fu, Yi]‘s Articles
[Guo, Deliang]‘s Articles
Related Copyright Policies
Null
Social Bookmarking
Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit

Items in IR are protected by copyright, with all rights reserved, unless otherwise indicated.

 

 

Valid XHTML 1.0!
Copyright © 2007-2017  北京大学医学部 - Feedback
Powered by CSpace