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学科主题基础医学
Receptor Interacting Protein 3 Suppresses Vascular Smooth Muscle Cell Growth by Inhibition of the Phosphoinositide 3-Kinase-Akt Axis
Li, Qian1,2; Li, Geng2; Lan, Xiaomei1,2; Zheng, Ming1; Chen, Kuang-Hueih3; Cao, Chun-Mei1; Xiao, Rui-Ping1,2,3
刊名JOURNAL OF BIOLOGICAL CHEMISTRY
2010-03-26
DOI10.1074/jbc.M109.071332
285期:13页:9535-9544
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology
研究领域[WOS]Biochemistry & Molecular Biology
关键词[WOS]NF-KAPPA-B ; ANGIOTENSIN-CONVERTING ENZYME ; RIP-LIKE KINASE ; NEOINTIMAL HYPERPLASIA ; BALLOON ANGIOPLASTY ; DEATH DOMAIN ; APOPTOSIS ; AKT ; PROLIFERATION ; RESTENOSIS
英文摘要

Proliferation of vascular smooth muscle cells (VSMCs) is a primary mechanism underlying cardiovascular proliferative disorders. Phosphoinositide 3-kinase (PI3K)-Akt (or protein kinase B) axis has been assigned at the center of pathways that regulate cell proliferation. Here we demonstrate that enhanced PI3K-Akt signaling by mitogenic stimulation or arterial injury profoundly elevates expression of receptor interacting protein 3 (RIP3) in primary cultured rat VSMCs and in vivo and that the up-regulation of RIP3 leads toVSMCgrowth arrest and apoptosis via inhibiting the PI3K-Akt signaling pathway, thereby alleviating balloon injury-induced neointimal formation. Specifically, mitogenic stimulation with platelet-derived growth factor-BB or angiotensin II leads to a profound increase in RIP3 expression, which is abolished by inhibition of PI3K or Akt, and increased PI3K-Akt signaling by expression of a constitutively active PI3K mutant also elevates RIP3 expression. Importantly, adenoviral overexpression of RIP3 not only triggers apoptosis but also causes cell cycle arrest at G(1)/G(0) phases that is associated with suppressed Akt activation. In sharp contrast, RIP3 gene silencing enhances serum- and platelet-derived growth factor-induced cell proliferation and Akt activation. In vivo adenoviral gene delivery of rat RIP3 (rRIP3) increased apoptosis and reduced VSMC proliferation, thus, effectively alleviating balloon injury-induced neointimal formation. The growth-suppressive and pro-apoptotic effects are independent of rRIP3 Ser/Thr kinase activity, because overexpression of a kinase-in-active mutant of rRIP3, similar to its wild type, is sufficient to induce growth arrest and apoptosis. These findings reveal a novel growth-suppressive action of RIP3, marking RIP3 as an important factor to prevent excessive mitogenic stimulation- or injury-induced vascular smooth muscle cells hyperplasia.

语种英语
WOS记录号WOS:000276165900027
引用统计
被引频次:19[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/400002259/65220
专题北京大学基础医学院_心血管所
北京大学基础医学院
作者单位1.Peking Univ, Inst Mol Med, Beijing 100083, Peoples R China
2.Peking Univ, Inst Cardiovasc Sci, Beijing 100083, Peoples R China
3.NIA, Cardiovasc Sci Lab, Baltimore, MD 21224 USA
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GB/T 7714
Li, Qian,Li, Geng,Lan, Xiaomei,et al. Receptor Interacting Protein 3 Suppresses Vascular Smooth Muscle Cell Growth by Inhibition of the Phosphoinositide 3-Kinase-Akt Axis[J]. JOURNAL OF BIOLOGICAL CHEMISTRY,2010,285(13):9535-9544.
APA Li, Qian.,Li, Geng.,Lan, Xiaomei.,Zheng, Ming.,Chen, Kuang-Hueih.,...&Xiao, Rui-Ping.(2010).Receptor Interacting Protein 3 Suppresses Vascular Smooth Muscle Cell Growth by Inhibition of the Phosphoinositide 3-Kinase-Akt Axis.JOURNAL OF BIOLOGICAL CHEMISTRY,285(13),9535-9544.
MLA Li, Qian,et al."Receptor Interacting Protein 3 Suppresses Vascular Smooth Muscle Cell Growth by Inhibition of the Phosphoinositide 3-Kinase-Akt Axis".JOURNAL OF BIOLOGICAL CHEMISTRY 285.13(2010):9535-9544.
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