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学科主题: 临床医学
题名:
Soluble epoxide hydrolase plays an essential role in angiotensin II-induced cardiac hypertrophy
作者: Ai, Ding1,4,5; Pang, Wei1; Li, Nan1; Xu, Ming2,3; Jones, Paul D.4,5,7; Yang, Jun4,5; Zhang, Youyi2,3; Chiamvimonvat, Nipavan6; Shyy, John Y. -J.8; Hammock, Bruce D.4,5; Zhu, Yi1
关键词: epoxyeicosatrienoic acid ; cardiomyocyte ; activator protein 1
刊名: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
发表日期: 2009-01-13
DOI: 10.1073/pnas.0811022106
卷: 106, 期:2, 页:564-569
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]: SENSITIVE K+ CHANNELS ; INNER MITOCHONDRIAL-MEMBRANE ; REGULATED KINASE PATHWAY ; JUN NH2-TERMINAL KINASE ; PRESSURE-OVERLOAD ; BLOOD-PRESSURE ; HEART-FAILURE ; ATP CHANNELS ; IN-VITRO ; HYPERTENSION
英文摘要:

Pathophysiological cardiac hypertrophy is one of the most common causes of heart failure. Epoxyeicosatrienoic acids, hydrolyzed and degraded by soluble epoxide hydrolase (sEH), can function as endothelium-derived hyperpolarizing factors to induce dilation of coronary arteries and thus are cardioprotective. In this study, we investigated the role of sEH in two rodent models of angiotensin II (Ang II)-induced cardiac hypertrophy. The protein level of sEH was elevated in the heart of both spontaneously hypertensive rats and Ang II-infused Wistar rats. Blocking the Ang II type 1 receptor with losartan could abolish this induction. Administration of a potent sEH inhibitor (sEHI) prevented the pathogenesis of the Ang II-induced hypertrophy, as demonstrated by decreased left-ventricular hypertrophy assessed by echocardiography, reduced cardiomyocyte size, and attenuated expression of hypertrophy markers, including atrial natriuretic factor and beta-myosin heavy chain. Because sEH elevation was not observed in exercise-or norepinephrine-induced hypertrophy, the sEH induction was closely associated with Ang II-induced hypertrophy. In vitro, Ang II upregulated sEH and hypertrophy markers in neonatal cardiomyocytes isolated from rat and mouse. Expression of these marker genes was elevated with adenovirus-mediated sEH overexpression but decreased with sEHI treatment. These results were supported by studies in neonatal cardiomyocytes from sEH(-/-) mice. Our results suggest that sEH is specifically upregulated by Ang II, which directly mediates Ang II-induced cardiac hypertrophy. Thus, pharmacological inhibition of sEH would be a useful approach to prevent and treat Ang II-induced cardiac hypertrophy.

语种: 英语
所属项目编号: 30570713 ; 30630032 ; R37 ; ES02710 ; P42 ; ES04699 ; ES05707 ; P42 ; ES04699 ; HL 85727 ; F32 HL078096
项目资助者: National Natural Science Foundation of China ; Major National Basic Research ; National Institute of Environmental Health Sciences ; National Institutes of Health ; National Heart, Lung, and Blood Institute Ruth L. Kirschstein National Service
WOS记录号: WOS:000262804000039
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59726
Appears in Collections:北京大学第三临床医学院_心血管内科_期刊论文

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作者单位: 1.Int Flavors & Fragrances Inc, Union Beach, NJ 07735 USA
2.Peking Univ, Dept Physiol & Pathophysiol, Beijing 100083, Peoples R China
3.Peking Univ, Hosp 3, Inst Vasc Med, Beijing 100083, Peoples R China
4.Peking Univ, Minist Educ, Key Lab Mol Cardiovasc Sci, Hlth Sci Ctr, Beijing 100083, Peoples R China
5.Univ Calif Davis, Dept Entomol, Davis, CA 95616 USA
6.Univ Calif Davis, Canc Res Ctr, Davis, CA 95616 USA
7.Univ Calif Davis, Univ Calif Med Ctr, Dept Cardiovasc Med, Davis, CA 95616 USA
8.Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA

Recommended Citation:
Ai, Ding,Pang, Wei,Li, Nan,et al. Soluble epoxide hydrolase plays an essential role in angiotensin II-induced cardiac hypertrophy[J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA,2009,106(2):564-569.
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