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学科主题: 基础医学
题名:
Suppression of pro-inflammatory adhesion molecules by PPAR-delta in human vascular endothelial cells
作者: 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
发表日期: 2008-02-01
DOI: 10.1161/ATVBAHA.107.149815
卷: 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
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/54739
Appears in Collections:基础医学院_心血管所_期刊论文

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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

Recommended Citation:
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.
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