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Effects of chemokine-like factor 1 on vascular smooth muscle cell migration and proliferation in vascular inflammation
Zhang, Tao1; Zhang, Xiaoming1; Yu, Weidong2; Chen, Jian3; Li, Qingle1; Jiao, Yang1; He, Peiying2; Shen, Chenyang1
关键词Chemokine-like Factor 1 Vascular Smooth Muscle Cell Migration And Proliferation Neointima Formation Atherosclerosis
刊名ATHEROSCLEROSIS
2013
DOI10.1016/j.atherosclerosis.2012.09.023
226期:1页:49-57
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Peripheral Vascular Disease
资助者National Natural Science Foundation of the People&prime ; s Republic of China ; National Natural Science Foundation of the People&prime ; s Republic of China
研究领域[WOS]Cardiovascular System & Cardiology
关键词[WOS]INTIMAL HYPERPLASIA ; LOWER-EXTREMITY ; DISEASE ; MECHANISMS ; ATHEROSCLEROSIS ; DYSFUNCTION ; EXPRESSION ; CYTOKINES ; ANTISENSE ; SURGERY
英文摘要

Objective: Vascular smooth muscle cell (VSMC) migration and proliferation are key components of vascular inflammation that may lead to atherosclerosis and restenosis, in which cytokines are considered as pivotal factors regarding recruitment of VSMC. A member of recently described family of chemokines, chemokine-like factor 1 (CKLF1), displays a wide spectrum of chemotaxis. This study investigated the role of CKLF1 in VSMC migration and proliferation during the process of vascular inflammation.

Methods and results: : The effects of CKLF1 on migration, proliferation and neointimal formation were investigated in cultured VSMCs, rat balloon injured arteries and human atherosclerotic plaques. CKLF1 overexpression greatly enhanced, whereas shRNA knockdown markedly retarded, VSMC migration and proliferation in vitro. In addition, CKLF1 protein accumulated preferentially in neointima of the injured rat arteries in vivo. CKLF1 overexpression resulted in a 2.5-fold increase in intimal thickness. In contrast, shRNA-mediated CKLF1 knockdown significantly suppressed neointima formation by 70% compared that in control group. Intriguingly, besides animal model, higher level of CKLF1 was observed in human atherosclerotic plaques than that in normal arteries.

Conclusion: CKLF1 plays an essential role in migration and proliferation of VSMCs, which in turn facilitated neointimal hyperplasia and atherosclerosis. Inhibition of CKLF1 activity provides a potential target for the prevention of atherosclerosis and restenosis. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

语种英语
所属项目编号30672039
资助者National Natural Science Foundation of the People&prime ; s Republic of China ; National Natural Science Foundation of the People&prime ; s Republic of China
WOS记录号WOS:000312807700010
引用统计
被引频次:6[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/400002259/60085
专题北京大学第二临床医学院_血管外科
作者单位1.Peking Univ, Peoples Hosp, Dept Vasc Surg, Beijing 100044, Peoples R China
2.Peking Univ, Peoples Hosp, Dept Cent Lab, Beijing 100044, Peoples R China
3.Chinese Acad Sci, Inst Elect, State Key Lab Transducer Technol, Beijing 100190, Peoples R China
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GB/T 7714
Zhang, Tao,Zhang, Xiaoming,Yu, Weidong,et al. Effects of chemokine-like factor 1 on vascular smooth muscle cell migration and proliferation in vascular inflammation[J]. ATHEROSCLEROSIS,2013,226(1):49-57.
APA Zhang, Tao.,Zhang, Xiaoming.,Yu, Weidong.,Chen, Jian.,Li, Qingle.,...&Shen, Chenyang.(2013).Effects of chemokine-like factor 1 on vascular smooth muscle cell migration and proliferation in vascular inflammation.ATHEROSCLEROSIS,226(1),49-57.
MLA Zhang, Tao,et al."Effects of chemokine-like factor 1 on vascular smooth muscle cell migration and proliferation in vascular inflammation".ATHEROSCLEROSIS 226.1(2013):49-57.
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