國家衛生研究院 NHRI:Item 3990099045/7977
English  |  正體中文  |  简体中文  |  全文笔数/总笔数 : 12145/12927 (94%)
造访人次 : 853840      在线人数 : 1264
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/3990099045/7977


    题名: Notch signaling prevents mucous metaplasia in mouse conducting airways during postnatal development
    作者: Tsao, PN;Wei, SC;Wu, MF;Huang, MT;Lin, HY;Lee, MC;Lin, KMC;Wang, IJ;Kaartinen, V;Yang, LT;Cardoso, WV
    贡献者: Institute of Cellular and Systems Medicine;Division of Medical Engineering Research
    摘要: Background and Aims: Goblet cell metaplasia and mucus overproduction contribute to the pathogenesis of chronic lung diseases, including asthma, chronic obstructive pulmonary disease. Notch signaling regulates cell fate decisions and plays a critical role in goblet cell differentiation in the gut epithelium. However it is unclear whether endogenous Notch influences goblet cell differentiation in airways. Methods: We inactivated Notch signaling conditionally in the lung using a Tgfb3-Cre deleter mouse line, which targets the airway epithelium in a mosaic fashion, and mice carrying floxed alleles of the Pofut1 gene, which encodes an O-fucosyltransferase essential for Notch-ligand binding. Immunohistochemistry, cell culture and transfection were used to analyze the lung phenotype and possible mechanism. Results: Mice were viable but showed an aberrant airway phenotype with decreased Clara cell number and marked goblet cell metaplasia during postnatal life. The phenotype was confirmed by a panel of goblet cell markers, showed no changes in cell proliferation or altered expression of proinflammatory cytokines and was associated with significant downregulation of Hes5. Luciferase reporter analysis suggested that Notch directly repressed MUC5AC transcription in lung epithelial cells. The same phenotype in mice in which the Notch transcriptional effector Rbpjk was deleted indicated the involvement of the canonical Notch pathway. Conclusions: The data suggested that during postnatal life Notch signaling is required to maintain the Clara cell phenotype and prevent goblet cell differentiation in proximal airways. Notch may be critical in regulating the response of the lung to environmental injurants or allergens that result in goblet cell metaplasia.
    日期: 2011-11
    關聯: Pediatric Research. 2011 Nov;70:560.
    Link to: http://dx.doi.org/10.1038/pr.2011.785
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0031-3998&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000208870100561
    显示于类别:[楊良棟] 會議論文/會議摘要
    [林名釗] 會議論文/會議摘要

    文件中的档案:

    档案 描述 大小格式浏览次数
    ISI000208870100561.pdf14KbAdobe PDF557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