English  |  正體中文  |  简体中文  |  Items with full text/Total items : 54367/62174 (87%)
Visitors : 15223039      Online Users : 155
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTHU 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
    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  Modulation of chemotactic and pro-inflammatory activities of endothelial progenitor cells by hepatocellular carcinoma

    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/81443

    Title: Modulation of chemotactic and pro-inflammatory activities of endothelial progenitor cells by hepatocellular carcinoma
    Authors: Yu-Tsung Shih;Mei-Cun Wang;Hsin-Hsin Peng;Ting-Fang Chen;Linyi Chen;Jang-Yang Chang;Jeng-Jiann Chiu
    教師: 陳令儀
    Date: 2012
    Publisher: Elsevier
    Relation: Cellular Signalling, Elsevier, Volume 24, Issue 3, MAR 2012, Pages 779-793
    Keywords: Endothelial progenitor cell
    Hepatocellular carcinoma
    MIP-3 alpha/CCR6 axis
    Abstract: Endothelial progenitor cells (EPCs) participate in the neovascularization processes in the development of hepatocellular carcinoma (HCC). We investigated whether interactions between EPCs and HCC cells affect chemotactic and pro-inflammatory activities of EPCs. Two distinct phenotypes of circulating EPCs, i.e., myeloid-derived EPCs (colony forming unit-endothelial cells, CFU-ECs) and outgrowth EPCs (endothelial-colony forming cells, ECFCs), were co-cultured with Huh7 and Hep3B cells by using transwell chamber and IBIDITM Culture-Inserts and μ-slide plates. Transwell and horizontal migration/invasion assays and time-lapse microscopy were used to monitor and analyze the migration and invasion of EPCs induced by these HCC cells. A human cytokine antibody array was used to compare protein expression profiles in EPCs and HCC cells. Flow cytometry and electromobility shift analysis were used to detect nuclear factor-κB (NF-κB)–DNA binding activity and pro-inflammatory adhesion molecule expression in EPCs. Ectopic full-length CC chemokine receptor 6 (CCR6) plasmid was used to transfect into ECFCs to investigate the role of CCR6 in HCC-induced EPC migration and invasion. The results show that co-culture with Huh7 and Hep3B cells induces the expression of endothelial cell (EC) markers KDR, Flt1, CD31 and VE-cadherin in CFU-ECs, but down-regulates the expressions of CD31 and VE-cadherin in ECFCs. These HCC cells induce migration and invasion of CFU-ECs, but not ECFCs, and do not affect the cell cycle distribution in these EPCs. Cytokine protein array identifies macrophage inflammatory protein-3α (MIP-3α) produced by HCC cells as a critical factor responsible for the HCC-induced chemotaxis of CFU-ECs, which highly express the specific MIP-3α counterreceptor CCR6. Overexpressing CCR6 in ECFCs significantly increases their chemotaxis in response to HCC cells. Co-culturing EPCs with HCC cells results in decreases in NF-κB binding activity and hence intracellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin expressions in EPCs. Our results indicate that HCC cells exert differential effects on CFU-ECs and ECFCs, with increased chemotaxis for CFU-ECs, but not ECFCs. This HCC-induced chemotaxis of CFU-ECs is mediated by MIP-3α produced by HCC cells, which targets to CCR6 on CFU-ECs. Tumors may provide a humoral microenvironment to attenuate the pro-inflammatory activity of EPCs, which might be associated with the tumor escape mechanism
    Relation Link: http://www.elsevier.com/
    URI: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/81443
    Appears in Collections:[生命科學系] 期刊論文
    [分子醫學研究所] 期刊論文
    [腦科學研究中心] 期刊論文

    Files in This Item:

    File Description SizeFormat


    SFX Query


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