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学科主题临床医学
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
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
2013-07-01
DOI10.1007/s00380-012-0291-0
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
WOS记录号WOS:000321768700014
项目编号30871066
资助机构National Natural Science Foundation of China
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/54871
专题北京大学第一临床医学院_心血管内科
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
推荐引用方式
GB/T 7714
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.
APA Dong, Xiao.,Ye, Xiaojin.,Song, Nana.,Zhao, Jing.,Di, Beibing.,...&Ding, Wenhui.(2013).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.HEART AND VESSELS,28(4),514-523.
MLA Dong, Xiao,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".HEART AND VESSELS 28.4(2013):514-523.
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