國家衛生研究院 NHRI:Item 3990099045/6369
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 922654      Online Users : 1217
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/3990099045/6369


    Title: Activation of HGF/c-Met signaling by ultrafine carbon particles and its contribution to alveolar type II cell proliferation
    Authors: Chang, CC;Chiu, JJ;Chen, SL;Huang, HC;Chiu, HF;Lin, BH;Yang, CY
    Contributors: Division of Environmental Health and Occupational Medicine
    Abstract: 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.
    Date: 2012-04
    Relation: 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
    Appears in Collections:[Others] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    SCP84859768175.pdf1306KbAdobe PDF265View/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