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学科主题基础医学
Blockade of the Ras-Extracellular Signal-Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22 alpha-Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia
Dong, Li-Hua1; Wen, Jin-Kun1; Liu, George5,6; McNutt, Michael A.4; Miao, Sui-Bing1; Gao, Rui1; Zheng, Bin1; Zhang, Hailin2; Han, Mei1
关键词smooth muscle 22 alpha Ras vascular smooth muscle cells proliferation neointimal hyperplasia
刊名ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
2010-04-01
DOI10.1161/ATVBAHA.109.200501
30期:4页:683-691
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]ACTIN-BINDING ; CAROTID ARTERIES ; RETINOIC ACID ; GENE DELIVERY ; PROTEIN ; DIFFERENTIATION ; EXPRESSION ; INJURY ; ACTIVATION ; CYCLE
英文摘要

Objective-Vascular smooth muscle cells (VSMCs) can switch between differentiated and dedifferentiated phenotypes, and this phenotype switch is believed to be essential for repair of vascular injury. We studied the inhibitory effect of smooth muscle 22 alpha (SM22 alpha) on VSMC proliferation in vitro and in vivo and explored the potential molecular mechanisms of this effect.

Methods and Results-By using coimmunoprecipitation and glutathione S-transferase pull-down assays, we have shown that SM22 alpha binds to Ras in SM22 alpha-overexpressed VSMCs in the presence or absence of platelet-derived growth factor-BB stimulation. SM22 alpha arrested cell cycle progression through segregation of Ras with Raf-1 and downregulation of the Raf-1-MEK1/2-extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase signaling cascade. The inhibitory effect of SM22 alpha on VSMC proliferation was verified in vivo. The infection of rat carotid arteries with recombinant adenovirus encoding SM22 alpha inhibited neointimal hyperplasia via suppression of the Raf-1-MEK1/2-extracellular signal-regulated kinase 1/2 signaling pathway.

Conclusion-These findings suggest that high expression of SM22 alpha inhibits cell proliferation via reduction of the response to mitogen stimuli in VSMCs and provide a novel mechanism by which VSMCs maintain their contractile phenotype and resist mitogenic stimuli in an SM22 alpha-dependent manner. (Arterioscler Thromb Vasc Biol. 2010; 30: 683-691.)

语种英语
WOS记录号WOS:000275712500010
项目编号30770787 ; 30670845 ; C2005000722 ; C2006000814 ; 2008CB517402
资助机构National Natural Science Foundation of China ; Hebei Province Natural Science Foundation ; "973" Program of China
引用统计
被引频次:33[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/400002259/61361
专题北京大学基础医学院_心血管所
作者单位1.Hebei Med Univ, Inst Basic Med, Dept Biochem & Mol Biol, Shijiazhuang 050017, Peoples R China
2.Hebei Med Univ, Inst Basic Med, Dept Pharmacol, Shijiazhuang 050017, Peoples R China
3.Peking Univ, Inst Cardiovasc Sci, Dept Physiol, Beijing 100871, Peoples R China
4.Peking Univ, Sch Basic Med Sci, Dept Pathol, Beijing 100871, Peoples R China
5.Peking Univ, Sch Basic Med Sci, China Adm Educ, Beijing 100871, Peoples R China
6.Peking Univ, Sch Basic Med Sci, Key Lab Cardiovasc Sci, Beijing 100871, Peoples R China
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Dong, Li-Hua,Wen, Jin-Kun,Liu, George,et al. Blockade of the Ras-Extracellular Signal-Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22 alpha-Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia[J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY,2010,30(4):683-691.
APA Dong, Li-Hua.,Wen, Jin-Kun.,Liu, George.,McNutt, Michael A..,Miao, Sui-Bing.,...&Han, Mei.(2010).Blockade of the Ras-Extracellular Signal-Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22 alpha-Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia.ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY,30(4),683-691.
MLA Dong, Li-Hua,et al."Blockade of the Ras-Extracellular Signal-Regulated Kinase 1/2 Pathway Is Involved in Smooth Muscle 22 alpha-Mediated Suppression of Vascular Smooth Muscle Cell Proliferation and Neointima Hyperplasia".ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY 30.4(2010):683-691.
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