國家衛生研究院 NHRI:Item 3990099045/9251
English  |  正體中文  |  简体中文  |  Items with full text/Total items : 12145/12927 (94%)
Visitors : 906061      Online Users : 677
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
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/9251


    Title: Activation of FGF1B promoter and FGF1 are involved in cardiogenesis through the signaling of PKC but not MAPK
    Authors: Lin, HY;Lee, DC;Wang, HD;Chi, YH;Chiu, IM
    Contributors: Institute of Cellular and Systems Medicine
    Abstract: Heart disease is the leading cause of human death in the 21st century. Heart transplantation is a promising way to treat this. Because donor resources are limited, cell-based therapy has been developed as an alternative. Therefore, genes that trigger cardiogenesis could have potential in the treatment of heart disease. FGF1 is reported to stimulate cardiomyocyte proliferation under conditions of myocardial infarction; but little is known about its function during cardiac differentiation. In this study, we established an in vitro cardiogenesis model through a reliable chemical induction protocol to determine whether FGF1 and its gene expression are involved in cardiogenesis. Oxytocin, a well-known hormone but also a cardiac differentiation inducer, was used in a mouse embryonic stem cell line E14Tg2a to achieve cardiac differentiation. After differentiation, beating cell clusters appeared and the expression of FGF1B mRNA was upregulated in the late differentiation stage (differentiation days 8-14). Interestingly, FGF1B expression patterns during cardiac differentiation were similar to those of a mature cardiomyocyte marker, cardiac troponin T. The blockage of FGF1-FGFR signaling reduced not only the appearance of beating cluster formation but also the expression levels of cardiomyocyte-associated genes. Moreover, by investigating FGF1 downstream signaling cascades, we observed that the efficiency of beating cluster formation was mainly regulated via the FGF1-FGFR-PKC signaling axis. Taken together, we provide evidence to support that FGF1 could regulate cardiogenesis primarily through the PKC signaling, but not through the MAPK signaling pathway.
    Date: 2015-12
    Relation: Stem Cells and Development. 2015 Dec;24(24):2853-2863.
    Link to: http://dx.doi.org/10.1089/scd.2015.0157
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1547-3287&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000366599600002
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84983189409
    Appears in Collections:[Ing-Ming Chiu] Periodical Articles
    [Ya-Hui Chi] Periodical Articles

    Files in This Item:

    File Description SizeFormat
    PUB26414172.pdf544KbAdobe PDF607View/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