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学科主题: 临床医学
题名:
Urotensin II promotes the production of LTC4 in rat aortic adventitial fibroblasts through NF-kappa B-5-LO pathway by p38 MAPK and ERK activations
作者: Dong, Xiao1; Ye, Xiaojin1; Song, Nana1; Zhao, Jing1; Di, Beibing1; Peng, Fen1; Tang, Chaoshu2; Ding, Wenhui1
关键词: Urotensin II ; Adventitial fibroblast ; 5-Lipoxygenase ; Leukotriene ; Vascular inflammation
刊名: HEART AND VESSELS
发表日期: 2013-07-01
DOI: 10.1007/s00380-012-0291-0
卷: 28, 期:4, 页:514-523
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: ENDOTHELIAL-CELLS ; RECEPTOR ; 5-LIPOXYGENASE ; EXPRESSION ; MICE ; ATHEROSCLEROSIS ; INFLAMMATION ; KNOCKOUT ; ANEURYSM
英文摘要:

Adventitia is the outer part of the arterial wall where the inflammatory response often occurs. Urotensin II (UII) is a potent vasoconstrictive peptide that also promotes the inflammatory process in patients with cardiovascular disease. Leukotriene C-4 (LTC4), a lipid mediator, was recently found to play a role in the inflammatory process in the artery. We hypothesized that the adventitia is one of the resources of LTC4 and that UII may promote LTC4 production through the 5-LO (5-lipoxygenase) pathway in adventitial fibroblasts. Rat adventitial fibroblasts were isolated and incubated in serum-free medium with either UII alone or in combination with inhibitors of p38 MAPK, ERK, and UII receptors. The expression of 5-LO was detected using real-time polymerase chain reaction and Western blot. The translocation and binding activity of nuclear factor (NF)-kappa B were measured using immunofluorescence and electrophoretic mobility shift assay, respectively. The production of LTC4 was measured by enzyme-linked immunosorbent assay. The results indicated that: (1) adventitial fibroblasts were a source of LTC4 production; (2) UII increased the expression of the 5-LO mRNA and the protein by NF-kappa B activation through p38 MAPK and ERK pathways; and (3) UII promoted the LTC4 release in fibroblasts through the 5-LO pathway by p38 MAPK and ERK activations. The 5-LO pathway mediates LTC4 production, which may be a new mechanism in the pathogenesis of the vascular adventitial inflammation caused by UII.

语种: 英语
所属项目编号: 30871066
项目资助者: National Natural Science Foundation of China
WOS记录号: WOS:000321768700014
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54871
Appears in Collections:北京大学第一临床医学院_心血管内科_期刊论文

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作者单位: 1.Peking Univ, Hosp 1, Dept Internal Med, Div Cardiol, Beijing 10034, Peoples R China
2.Peking Univ, Dept Physiol & Pathophysiol, Beijing 100191, Peoples R China

Recommended Citation:
Dong, Xiao,Ye, Xiaojin,Song, Nana,et al. Urotensin II promotes the production of LTC4 in rat aortic adventitial fibroblasts through NF-kappa B-5-LO pathway by p38 MAPK and ERK activations[J]. HEART AND VESSELS,2013,28(4):514-523.
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