國家衛生研究院 NHRI:Item 3990099045/4432
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 857533      線上人數 : 604
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
搜尋範圍 查詢小技巧：
  • 您可在西文檢索詞彙前後加上"雙引號"，以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋，建議至進階搜尋限定作者欄位，可獲得較完整資料
    •  進階搜尋
    主頁 ‧ 登入 ‧ 上傳 ‧ 說明 ‧ 關於NHRI ‧ 管理 到手機版


    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/4432


    題名: Leukotriene C-4 induces TGF-beta(1) production in airway epithelium via p38 kinase pathway
    其他題名: Leukotriene C4 induces TGF-β1 production in airway epithelium via p38 kinase pathway
    作者: Perng, DW;Wu, YC;Chang, KT;Wu, MT;Chiou, YC;Su, KC;Perng, RP;Lee, YC
    貢獻者: Division of Molecular and Genomic Medicine
    摘要: Cysteinyl leukotrienes (CysLTs) play an important role in the pathogenesis of airway remodeling. We investigated the interaction between epithelium and CysLTC(4), and the contribution of this interaction to airway fibrosis. Human airway epithelial cells were grown on air-liquid interface culture inserts. CysLTC(4) was employed to stimulate the cells. Conditioned medium following CysLTC(4) stimulation was coincubated with human lung fibroblasts. Our results have demonstrated that CysLTC(4) stimulates airway epithelial cells, through a p38 mitogen-activated protein kinase (MAPK) activation mechanism, to produce transforming growth factor beta(1) (TGF-beta(1)), which results in fibroblast proliferation. The selective p38 MAPK inhibitor S203580 successfully inhibits p38 MARK phosphorylation and subsequent TGF-beta(1) production. CysLT(1) receptor antagonist montelukast and corticosteroid inhibit TGF-beta(1) production at the mRNA and protein levels. When treated with LTC4, the conditioned medium from epithelial cells enhances fibroblast proliferation, this mitogenic effect being attributed to TGF-beta(1) and LTC4 remaining in the culture medium. In addition, LTC4 itself acts as a potential growth factor for lung fibroblasts. These data indicate that interactions between LTC4 and airway epithelial cells may contribute to the pathogenesis of airway remodeling. Early intervention to stop these processes may be useful in preventing airway fibrosis in chronic allergic inflammation.
    日期: 2006-01
    關聯: American Journal of Respiratory Cell and Molecular Biology. 2006 Jan;34(1):101-107.
    Link to: http://dx.doi.org/10.1165/rcmb.2005-0068OC
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1044-1549&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000234390600012
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=29944436527
    顯示於類別:[其他] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    ISI000234390600012.pdf181KbAdobe PDF415檢視/開啟


    在NHRI中所有的資料項目都受到原著作權保護.

    TAIR相關文章

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