國家衛生研究院 NHRI:Item 3990099045/3615
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 859785      在线人数 : 831
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜寻范围 查询小技巧：
  • 您可在西文检索词汇前后加上"双引号"，以获取较精准的检索结果
  • 若欲以作者姓名搜寻，建议至进阶搜寻限定作者字段，可获得较完整数据
    •  进阶搜寻
    主页 ‧ 登入 ‧ 上传 ‧ 说明 ‧ 关于NHRI ‧ 管理 到手机版


    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/3615


    题名: Ligand-activated peroxisome proliferator-activated receptor-gamma protects against ischemic cerebral infarction and neuronal apoptosis by 14-3-3 epsilon upregulation
    其它题名: Ligand-Activated Peroxisome Proliferator-Activated Receptor-gamma Protects Against Ischemic Cerebral Infarction and Neuronal Apoptosis by 14-3-3 is an element of Upregulation
    作者: Wu, JS;Cheung, WM;Tsai, YS;Chen, YT;Fong, WH;Tsai, HD;Chen, YC;Liou, JY;Shyue, SK;Chen, JJ;Chen, YE;Maeda, N;Wu, KK;Lin, TN
    贡献者: Institute of Cellular and Systems Medicine
    摘要: Background-Thiazolidinediones have been reported to protect against ischemia-reperfusion injury. Their protective actions are considered to be peroxisome proliferator-activated receptor-γ (PPAR-γ)-dependent; however, it is unclear how PPAR-γ activation confers resistance to ischemia-reperfusion injury. Methods and Results-We evaluated the effects of rosiglitazone or PPAR-γ overexpression on cerebral infarction in a rat model and investigated the antiapoptotic actions in the N2-A neuroblastoma cell model. Rosiglitazone or PPAR-γ overexpression significantly reduced infarct volume. The protective effect was abrogated by PPAR-γ small interfering RNA. In mice with knock-in of a PPAR-γ dominant-negative mutant, infarct volume was enhanced. Proteomic analysis revealed that brain 14-3-3ε was highly upregulated in rats treated with rosiglitazone. Upregulation of 14-3-3ε was abrogated by PPAR-γ small interfering RNA or antagonist. Promoter analysis and chromatin immunoprecipitation revealed that rosiglitazone induced PPAR-γ binding to specific regulatory elements on the 14-3-3ε promoter and thereby increased 14-3-3ε transcription. 14-3-3ε Small interfering RNA abrogated the antiapoptotic actions of rosiglitazone or PPAR-γ overexpression, whereas 14-3-3ε recombinant proteins rescued brain tissues and N2-A cells from ischemia-induced damage and apoptosis. Elevated 14-3-3ε enhanced binding of phosphorylated Bad and protected mitochondrial membrane potential. Conclusions-Ligand-activated PPAR-γ confers resistance to neuronal apoptosis and cerebral infarction by driving 14-3-3ε transcription. 14-3-3e Upregulation enhances sequestration of phosphorylated Bad and thereby suppresses apoptosis.
    日期: 2009-03-03
    關聯: Circulation. 2009 Mar 3;119(8):1124-1134.
    Link to: http://dx.doi.org/10.1161/circulationaha.108.812537
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0009-7322&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000263772100010
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=62649096776
    显示于类别:[伍焜玉] 期刊論文
    [劉俊揚] 期刊論文

    文件中的档案:

    档案 描述 大小格式浏览次数
    SCP62649096776.pdf606KbAdobe PDF871检视/开启


    在NHRI中所有的数据项都受到原著作权保护.

    TAIR相关文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - 回馈