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学科主题: 基础医学
题名:
Cartilage Oligomeric Matrix Protein Maintains the Contractile Phenotype of Vascular Smooth Muscle Cells by Interacting With alpha(7)beta(1) Integrin
作者: Wang, Li1; Zheng, Jingang3; Du, Yaoyao1; Huang, Yaqian1; Li, Jing1; Liu, Bo1; Liu, Chuan-ju4,5; Zhu, Yi1; Gao, Yuansheng1; Xu, Qingbo6; Kong, Wei1; Wang, Xian1
关键词: smooth muscle cells ; phenotype ; COMP ; integrin ; neointima
刊名: CIRCULATION RESEARCH
发表日期: 2010-02-19
DOI: 10.1161/CIRCRESAHA.109.202762
卷: 106, 期:3, 页:514-525
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Cardiac & Cardiovascular Systems ; Hematology ; Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology ; Hematology
关键词[WOS]: EXPRESSION ; ADHESION ; DIFFERENTIATION ; MODULATION ; ACTIN ; ATHEROSCLEROSIS ; TRANSDUCTION ; MAINTENANCE ; MYOCARDIN ; DYNAMICS
英文摘要:

Rational: Vascular smooth muscle cells (VSMCs) switching from a contractile/differentiated to a synthetic/dedifferentiated phenotype has an essential role in atherosclerosis, postangioplastic restenosis and hypertension. However, how normal VSMCs maintain the differentiated state is less understood.

Objective: We aimed to indentify the effect of cartilage oligomeric matrix protein (COMP), a normal vascular extracellular matrix, on modulation of VSMCs phenotype.

Methods and Results: We demonstrated that COMP was associated positively with the expression of VSMC differentiation marker genes during phenotype transition. Knockdown of COMP by small interfering (si) RNA favored dedifferentiation. Conversely, adenoviral overexpression of COMP markedly suppressed platelet-derived growth factor-BB-elicited VSMC dedifferentiation, characterized by altered VSMC morphology, actin fiber organization, focal adhesion assembly, and the expression of phenotype-dependent markers. Whereas alpha(7) integrin coimmunoprecipitated with COMP in normal rat VSMCs and vessels, neutralizing antibody or siRNA against alpha(7) integrin inhibited VSMC adhesion to COMP, which indicated that alpha(7)beta(1) integrin is a potential receptor for COMP. As well, blocking or interference by siRNA of alpha(7) integrin completely abolished the effect of COMP on conserving the contractile phenotype. In accordance, ectopic adenoviral overexpression of COMP greatly retarded VSMC phenotype switching, rescued contractility of carotid artery ring, and inhibited neointima formation in balloon-injured rats.

Conclusions: Our data suggest that COMP is essential for maintaining a VSMC contractile phenotype and the protective effects of COMP are mainly mediated through interaction with alpha(7)beta(1) integrin. Investigations to identify the factors affecting the expression and integrity of COMP may provide a novel therapeutic target for vascular disorders. (Circ Res. 2010;106:514-525.)

语种: 英语
所属项目编号: 30670849 ; 30870993 ; 30821001 ; 30770865 ; 2006CB503802 ; 307001
项目资助者: National Natural Science Foundation of the People&prime ; s Republic of China ; Natural Science Foundation of Beijing ; Ministry of Education of China ; Chinese Ministry of Education ; Chang Jiang Scholars Program
WOS记录号: WOS:000274651400014
Citation statistics:
内容类型: 期刊论文
版本: 出版稿
URI标识: http://ir.bjmu.edu.cn/handle/400002259/51781
Appears in Collections:基础医学院_生理学与病理生理学系_期刊论文

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作者单位: 1.NYU, Sch Med, Dept Cell Biol, New York, NY 10003 USA
2.Minist Educ, Key Lab Mol Cardiovasc Sci, Beijing, Peoples R China
3.NYU, Sch Med, Dept Orthopaed Surg, New York, NY 10003 USA
4.Peking Univ, Basic Med Coll, Dept Physiol & Pathophysiol, Sch Basic Med Sci, Beijing 100191, Peoples R China
5.China Japan Friendship Hosp, Dept Cardiol, Beijing, Peoples R China
6.Kings Coll London, British Heart Fdn Ctr, Div Cardiovasc, London, England

Recommended Citation:
Wang, Li,Zheng, Jingang,Du, Yaoyao,et al. Cartilage Oligomeric Matrix Protein Maintains the Contractile Phenotype of Vascular Smooth Muscle Cells by Interacting With alpha(7)beta(1) Integrin[J]. CIRCULATION RESEARCH,2010,106(3):514-525.
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