國家衛生研究院 NHRI:Item 3990099045/4432
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 909748      Online Users : 853
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
    •  Adv. Search
    Home ‧ Login ‧ Upload ‧ Help ‧ About ‧ Administer Goto mobile version


    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/4432


    Title: Leukotriene C-4 induces TGF-beta(1) production in airway epithelium via p38 kinase pathway
    Other Titles: Leukotriene C4 induces TGF-β1 production in airway epithelium via p38 kinase pathway
    Authors: Perng, DW;Wu, YC;Chang, KT;Wu, MT;Chiou, YC;Su, KC;Perng, RP;Lee, YC
    Contributors: Division of Molecular and Genomic Medicine
    Abstract: 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.
    Date: 2006-01
    Relation: 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
    Appears in Collections:[Others] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    ISI000234390600012.pdf181KbAdobe PDF416View/Open


    All items in NHRI are protected by copyright, with all rights reserved.

    Related Items in TAIR

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