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学科主题基础医学
Suppression of pro-inflammatory adhesion molecules by PPAR-delta in human vascular endothelial cells
Fan, Yanbo1,2,3; Wang, Ying1,2,3; Tang, Zhihui1,2,3; Zhang, Hong1,2,3; Qin, Xiaomei1,2,3; Zhu, Yi1,2,3; Guan, Youfei1,2,3; Wang, Xian1,2,3; Staels, Bart4; Chien, Shu5,6,7,8; Wang, Nanping1,2,3
关键词Adhesion Molecules Nuclear Receptor Endothelium Gene Expression Reactive Oxygen Species
刊名ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
2008-02-01
DOI10.1161/ATVBAHA.107.149815
28期:2页:315-321
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Hematology ; Peripheral Vascular Disease
研究领域[WOS]Hematology ; Cardiovascular System & Cardiology
关键词[WOS]ACTIVATED-RECEPTOR-DELTA ; NF-KAPPA-B ; OXIDATIVE STRESS ; FATTY-ACIDS ; TRANSCRIPTIONAL REPRESSION ; CRITICAL ROLES ; GAMMA ; ALPHA ; BETA ; ATHEROSCLEROSIS
英文摘要

Objective-Endothelial activation is implicated in atherogenesis and diabetes. The role of peroxisome proliferator-activated receptor-delta (PPAR-delta) in endothelial activation remains poorly understood. In this study, we investigated the anti-inflammatory effect of PPAR-delta and the mechanism involved.

Methods and Results-In human umbilical vein endothelial cells (HUVECs), the synthetic PPAR-delta ligands GW0742 and GW501516 significantly inhibited tumor necrosis factor (TNF)-alpha-induced expression of vascular cell adhesion molecule-1 and E-selectin (assayed by real-time RT-PCR and Northern blotting), as well as the ensuing endothelial-leukocyte adhesion. Activation of PPAR-delta upregulated the expression of antioxidant genes superoxide dismutase 1, catalase, and thioredoxin and decreased reactive oxygen species production in ECs. Chromatin immunoprecipitation assays showed that GW0742 switched the association of BCL-6, a transcription repressor, from PPAR-delta to the vascular cell adhesion molecule ( VCAM)-1 promoter. Small interfering RNA reduced endogenous PPAR-delta expression but potentiated the suppressive effect of GW0742 on EC activation, which suggests that the nonliganded PPAR-delta may have an opposite effect.

Conclusions-We have demonstrated that ligand activation of PPAR-delta in ECs has a potent antiinflammatory effect, probably via a binary mechanism involving the induction of antioxidative genes and the release of nuclear corepressors. PPAR-delta agonists may have a potential for treating inflammatory diseases such as atherosclerosis and diabetes.

语种英语
WOS记录号WOS:000252707400018
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被引频次:89[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/400002259/54739
专题北京大学基础医学院_心血管所
北京大学基础医学院
北京大学口腔医学院_第二门诊部
作者单位1.Univ Lille 2, Fac Med, Lille, France
2.Peking Univ, Ctr Diabet, Beijing 100871, Peoples R China
3.Univ Lille 2, Fac Pharm, Lille, France
4.Peking Univ, Hlth Sci Ctr, Inst Cardiovasc Sci, Beijing 100083, Peoples R China
5.Peking Univ, Key Lab Mol Cardiovasc Sci, Beijing 100083, Peoples R China
6.Inst Pasteur, INSERM, U545, Lille, France
7.Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA
8.Univ Calif San Diego, Dept Med, La Jolla, CA 92093 USA
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GB/T 7714
Fan, Yanbo,Wang, Ying,Tang, Zhihui,et al. Suppression of pro-inflammatory adhesion molecules by PPAR-delta in human vascular endothelial cells[J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY,2008,28(2):315-321.
APA Fan, Yanbo.,Wang, Ying.,Tang, Zhihui.,Zhang, Hong.,Qin, Xiaomei.,...&Wang, Nanping.(2008).Suppression of pro-inflammatory adhesion molecules by PPAR-delta in human vascular endothelial cells.ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY,28(2),315-321.
MLA Fan, Yanbo,et al."Suppression of pro-inflammatory adhesion molecules by PPAR-delta in human vascular endothelial cells".ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 28.2(2008):315-321.
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