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PGC-1 alpha attenuates neointimal formation via inhibition of vascular smooth muscle cell migration in the injured rat carotid artery
Qu, Aijuan1; Jiang, Changtao1; Xu, Mingjiang1; Zhang, Yan2; Zhu, Yi1; Xu, Qingbo3; Zhang, Chenyu2; Wang, Xian1
关键词Restenosis Antioxidants Smooth Muscle Cells Metabolic Syndrome Peroxisome Proliferator-activated Receptor-gamma Coactivator-1 Alpha
刊名AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
2009-09-01
DOI10.1152/ajpcell.00469.2008
297期:3页:C645-C653
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology ; Physiology
研究领域[WOS]Cell Biology ; Physiology
关键词[WOS]KAPPA-B ACTIVATION ; MITOCHONDRIAL BIOGENESIS ; ENDOTHELIAL-CELLS ; PGC-1 COACTIVATORS ; ENERGY-METABOLISM ; OXIDATIVE STRESS ; GENE-EXPRESSION ; GROWTH ; MECHANISMS ; DISEASE
英文摘要

Qu A, Jiang C, Xu M, Zhang Y, Zhu Y, Xu Q, Zhang C, Wang X. PGC-1 alpha attenuates neointimal formation via inhibition of vascular smooth muscle cell migration in the injured rat carotid artery. Am J Physiol Cell Physiol 297: C645-C653, 2009. First published June 24, 2009; doi:10.1152/ajpcell.00469.2008.-Oxidative stress contributes significantly to the migration of vascular smooth muscle cells (VSMCs), the major pathogenic process of vascular diseases, but the mechanism remains unclear. In the present study, we explored the role of peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1 alpha), a major regulator of mitochondrial biogenesis and energy balance, in VSMC migration in vitro and in vivo. Overexpression of PGC-1 alpha in cultured VSMCs led to a 74.5% reduction of migration activity and mitochondrial ROS generation by the increased expression of antioxidative proteins such as SOD-2 in the mitochondria. The knockdown of PGC-1 alpha by specific small interfering (si)RNA markedly augmented VSMC migration activity and greatly reduced mitochondrial antioxidative protein expression. Furthermore, knockdown of SOD-2 expression by siRNA greatly reversed the inhibitory effect of PGC-1 alpha overexpression on VSMC migration. In a rat carotid balloon injury model, adenovirus-mediated overexpression of PGC-1 alpha greatly reduced neointimal formation (ratio of intima to media: 0.78 +/- 0.09 vs. 1.45 +/- 0.18 in the adenovirus + green fluorescent protein gene-transfected group). Moreover, the expression of SOD-2 was significantly increased in vivo in local vessels after injury in the PGC-1 alpha-overexpressing group. These data strongly suggest that PGC-1 alpha inhibits VSMC migration and neointimal formation after vascular injury in rats, mainly by upregulating the expression of the mitochondrial antioxidant enzyme SOD-2.

语种英语
WOS记录号WOS:000269584200017
项目编号2006CB503802 ; 30821001 ; 307001
资助机构Major National Basic Research Program of the People&prime ; s Republic of China ; National Natural Science Foundation of the People&prime ; s Repulbic of China ; Key Grant Project of Chinese Ministry of Education ; Chang Jiang Scholars Program
引用统计
被引频次:20[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/400002259/55885
专题北京大学基础医学院
作者单位1.Peking Univ, Dept Physiol & Pathophysiol, Sch Basic Med Sci, Key Lab Mol Cardiovas Sci,Minist Educ, Beijing 100191, Peoples R China
2.Nanjing Univ, Sch Life Sci, State Key Lab Pharmaceut Biotechnol, Jiangsu Diabet Ctr, Nanjing 210008, Peoples R China
3.Kings Coll London, James Black Ctr, Div Cardiovasc, London WC2R 2LS, England
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Qu, Aijuan,Jiang, Changtao,Xu, Mingjiang,et al. PGC-1 alpha attenuates neointimal formation via inhibition of vascular smooth muscle cell migration in the injured rat carotid artery[J]. AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY,2009,297(3):C645-C653.
APA Qu, Aijuan.,Jiang, Changtao.,Xu, Mingjiang.,Zhang, Yan.,Zhu, Yi.,...&Wang, Xian.(2009).PGC-1 alpha attenuates neointimal formation via inhibition of vascular smooth muscle cell migration in the injured rat carotid artery.AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY,297(3),C645-C653.
MLA Qu, Aijuan,et al."PGC-1 alpha attenuates neointimal formation via inhibition of vascular smooth muscle cell migration in the injured rat carotid artery".AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY 297.3(2009):C645-C653.
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