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学科主题: 基础医学
题名:
Pro-inflammatory Macrophages suppress PPAR gamma activity in Adipocytes via S-nitrosylation
作者: Yin, Ruiying1,2; Fang, Li1,2; Li, Yingjia1,2; Xue, Peng3; Li, Yazi3; Guan, Youfei4; Chang, Yongsheng5,6; Chen, Chang3; Wang, Nanping1,2,4
关键词: PPAR gamma ; S-nitrosylation ; Macrophage ; Adipose tissue ; Insulin resistance
刊名: FREE RADICAL BIOLOGY AND MEDICINE
发表日期: 2015-12-01
DOI: 10.1016/j.freeradbiomed.2015.10.406
卷: 89, 页:895-905
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Endocrinology & Metabolism
研究领域[WOS]: Biochemistry & Molecular Biology ; Endocrinology & Metabolism
关键词[WOS]: ACTIVATED-RECEPTOR-GAMMA ; NITRIC-OXIDE SYNTHASE ; ADIPOSE-TISSUE MACROPHAGES ; INSULIN-RESISTANCE ; OXIDATIVE STRESS ; PROTEIN DENITROSYLATION ; TARGETED DISRUPTION ; METABOLIC SYNDROME ; BINDING PROTEIN ; OBESITY
英文摘要:

Peroxisome proliferator-activated receptor-gamma (PPAR gamma) is a ligand-activated nuclear receptor and plays an essential role in insulin signaling. Macrophage infiltration into adipose tissue is a character of metabolic inflammation and closely related to insulin resistance in type 2 diabetes. The mechanism by which pro-inflammatory macrophages cause insulin resistance remains to be elucidated. Here we showed that coculture with macrophages significantly suppressed the transcriptional activity of PPAR gamma on its target genes in 3T3-L1 preadipocytes and diabetic primary adipocytes, depending on inducible nitric oxide synthase (iNOS). We further showed that PPAR gamma underwent S-nitrosylation in response to nitrosative stress. Mass-spectrometry and site-directed mutagenesis revealed that S-nitrosylation at cysteine 168 was responsible for the impairment of PPAR gamma function. Extended exposure to NO instigated the proteasome-dependent degradation of PPAR gamma. Consistently, in vivo evidence revealed an association of the decreased PPAR gamma protein level with increased macrophage infiltration in visceral adipose tissue (VAT) of obese diabetic db/db mice. Together, our results demonstrated that pro-inflammatory macrophages suppressed PPAR gamma activity in adipocytes via S-nitrosylation, suggesting a novel mechanism linking metabolic inflammation with insulin resistance. (C) 2015 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: 31430045 ; 81470373 ; 81220108005 ; 31225012 ; 2011CB910900 ; 2012CB911000
项目资助者: National Natural Science Foundation of China ; National Basic Research Program of China
WOS记录号: WOS:000366355800084
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/67578
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.Peking Union Med Coll, Beijing 100005, Peoples R China
2.Peking Univ, Ctr Diabet, Beijing 100191, Peoples R China
3.Peking Univ, Inst Cardiovasc Sci, Beijing 100191, Peoples R China
4.Chinese Acad Sci, Inst Biophys, Beijing 100101, Peoples R China
5.Dalian Med Univ, Adv Inst Med Sci, Dalian 116044, Peoples R China
6.Chinese Acad Med Sci, Inst Basic Med Sci, Natl Lab Med Mol Biol, Beijing 100005, Peoples R China

Recommended Citation:
Yin, Ruiying,Fang, Li,Li, Yingjia,et al. Pro-inflammatory Macrophages suppress PPAR gamma activity in Adipocytes via S-nitrosylation[J]. FREE RADICAL BIOLOGY AND MEDICINE,2015,89:895-905.
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