國家衛生研究院 NHRI:Item 3990099045/6369
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 916642      線上人數 : 1488
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/3990099045/6369


    題名: Activation of HGF/c-Met signaling by ultrafine carbon particles and its contribution to alveolar type II cell proliferation
    作者: Chang, CC;Chiu, JJ;Chen, SL;Huang, HC;Chiu, HF;Lin, BH;Yang, CY
    貢獻者: Division of Environmental Health and Occupational Medicine
    摘要: Activation of HGF/c-Met signaling by ultrafine carbonparticles and its contribution to alveolar type II cell proliferation. AmJ Physiol Lung Cell Mol Physiol 302: L755–L763, 2012. First pub-lished January 13, 2012; doi:10.1152/ajplung.00350.2011.—Hepato-cyte growth factor (HGF) is a potent mitogen and motogen for variousepithelial cells. The present study aimed to explore the role of HGFand c-Met receptor in ultrafine carbon particle-induced alveolar typeII epithelial (type II) cell proliferation. ICR mice were intratracheallyinstilled with 100 g ultrafine carbon black (ufCB) and killed at 21,48, and 72 days postexposure to examine type II cell proliferation,HGF release, and c-Met activation. In vivo and in vitro applications ofneutralizing anti-HGF antibody were used to investigate the causalrole of HGF in cell proliferation. The Met kinase inhibitor SU11274and extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitorPD98059 were used to delineate the involvement of c-Met/ERK1/2 inrat L2 pulmonary epithelial cell proliferation. The results demon-strated that in vivo exposure to 100 g ufCB caused increased HGFin bronchoalveolar lavage fluid, as well as increased HGF production,c-Met phosphorylation, and cell proliferation in type II cells. In vitrostudy revealed that ufCB caused a dose-dependent increase in HGFrelease, c-Met phosphorylation, and cell proliferation. Importantly,treatment with the neutralizing anti-HGF antibody significantlyblocked ufCB-induced in vivo and in vitro type II cell proliferation.Moreover, SU11274 and PD98059 significantly reduced ufCB-in-creased L2 cell proliferation. Results from Western blotting demon-strated that SU11274 successfully suppressed ufCB-induced phos-phorylation of c-Met and ERK1/2. In summary, the activation ofHGF/c-Met signaling is a major pathway involved in ufCB-inducedtype II cell proliferation.
    日期: 2012-04
    關聯: American Journal of Physiology - Lung Cellular and Molecular Physiology. 2012 Apr;302(8):L755-L763.
    Link to: http://dx.doi.org/10.1152/ajplung.00350.2011
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1040-0605&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000302918700006
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84859768175
    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
    SCP84859768175.pdf1306KbAdobe PDF264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