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IR@PKUHSC  > 北京大学第二临床医学院  > 血管外科  > 期刊论文
学科主题: 临床医学
题名:
Disruption of TGF-beta signaling in smooth muscle cell prevents elastase-induced abdominal aortic aneurysm
作者: Gao, Fu1; Chambon, Pierre2,3; Offermanns, Stefan4; Tellides, George5; Kong, Wei6; Zhang, Xiaoming1; Li, Wei1
关键词: Aneurysm ; TGF-beta ; Smooth muscle cell ; Elastase
刊名: BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
发表日期: 2014-11-07
DOI: 10.1016/j.bbrc.2014.10.053
卷: 454, 期:1, 页:137-143
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Biochemistry & Molecular Biology ; Biophysics
研究领域[WOS]: Biochemistry & Molecular Biology ; Biophysics
关键词[WOS]: TRANSFORMING GROWTH-FACTOR-BETA-1 ; MATRIX METALLOPROTEINASE-2 ; INTERLEUKIN-6 EXPRESSION ; PHENOTYPIC MODULATION ; MARFAN-SYNDROME ; PATHOGENESIS ; FIBROBLASTS ; MANAGEMENT ; APOPTOSIS ; MODEL
英文摘要:

Transforming growth factor-beta (TGF-beta) signaling has been significantly implicated in the pathogenesis of aneurysm, prominently the initiation and progression of abdominal aortic aneurysm (AAA). Vascular smooth muscle cell (SMC) is the principal resident cell in aortic wall and is essential for its structure and function. However, the role of TGF-beta, pathway in SMC for the formation of AAA remains unknown. Therefore, the goal of the present study was to investigate the effect of TGF-beta pathway in SMC for AAA pathogenesis, by using a genetical smooth muscle-specific (SM-specific) TGF-beta type II receptor (Tgfbr2) disruption animal model. Mice deficient in the expression of Tgfbr2 (MyhCre.Tgfbr2(f/f) and Myh-Cre.Tgfbr2(WT/f)) and their corresponding wild-type background mice (MyhCre.Tgfbr2(WT/WT)) underwent AAA induction by infrarenal peri-adventitial application of elastase. Fourteen days after elastase treatment, the aortas were analyzed and indicated that disruption of 1 or 2 alleles of Tgfbr2 in SMC provided markedly step-wise protection from AAA formation. And elastin degradation, medial SMC loss, macrophage infiltration, and matrix metalloproteinases (MMP) expression were all significantly reduced in Tgfbr2 deletion mice. Our study demonstrated, for the first time, that the TGF-beta signaling pathway in SMC plays a critical role in AAA and disruption can prevent the aneurysm formation. (C) 2014 Elsevier Inc. All rights reserved.

语种: 英语
所属项目编号: 2118000537 ; 2109000075
项目资助者: Peking University People&prime ; s Hospital Research and Development Funds grant ; Specialized Research Fund for the Doctoral Program of Higher Education of China
WOS记录号: WOS:000346693500024
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51919
Appears in Collections:北京大学第二临床医学院_血管外科_期刊论文

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作者单位: 1.ILLKIRCH, Inst Clin Souris, Strasbourg, France
2.Peking Univ, Peoples Hosp, Dept Vasc Surg, Beijing 100044, Peoples R China
3.Coll France, Inst Genet & Biol Mol & Cellulaire, CNRS UMR7104, ULP,INSERM U596, Strasbourg, France
4.Max Planck Inst Heart & Lung Res, Dept Pharmacol, Bad Nauheim, Germany
5.Yale Univ, Sch Med, Dept Surg, Interdept Program Vasc Biol & Therapeut, New Haven, CT 06510 USA
6.Peking Univ, Basic Med Coll, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China

Recommended Citation:
Gao, Fu,Chambon, Pierre,Offermanns, Stefan,et al. Disruption of TGF-beta signaling in smooth muscle cell prevents elastase-induced abdominal aortic aneurysm[J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS,2014,454(1):137-143.
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