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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/32286


    標題: Plasminogen/thrombomodulin signaling enhances VEGF expression to promote cutaneous wound healing
    作者: Cheng, Tsung-Lin
    Chen, Po-Ku
    Huang, Wei-Kai
    Kuo, Cheng-Hsiang
    Cho, Chia-Fong
    Wang, Kuan-Chieh
    Shi, Guey-Yueh
    Wu, Hua-Lin
    Lai, Chao-Han
    貢獻者: Kaohsiung Med Univ, Sch Med, Dept Physiol, Coll Med
    Kaohsiung Med Univ, Kaohsiung Med Univ Hosp, Coll Med, Orthopaed Res Ctr
    Kaohsiung Med Univ Hosp, Dept Med Res
    Natl Cheng Kung Univ, Cardiovasc Res Ctr
    Natl Cheng Kung Univ, Dept Biochem & Mol Biol, Coll Med
    Natl Cheng Kung Univ, Inst Basic Med Sci, Coll Med
    Natl Cheng Kung Univ, Dept Med Lab Sci & Biotechnol, Coll Med
    Natl Cheng Kung Univ, Coll Med, Dept Food Safety Hyg & Risk Management
    Chia Nan Univ Pharm & Sci, Coll Recreat & Hlth Management, Dept Tourism Management
    Natl Cheng Kung Univ, Natl Cheng Kung Univ, Dept Surg, Coll Med
    關鍵字: Plasminogen
    Thrombomodulin
    VEGF
    Wound healing
    日期: 2018-12
    上傳時間: 2019-11-15 15:48:10 (UTC+8)
    出版者: SPRINGER HEIDELBERG
    摘要: Plasminogen (Plg) and thrombomodulin (TM) are glycoproteins well known for fibrinolytic and anticoagulant functions, respectively. Both Plg and TM are essential for wound healing. However, their significance during the reparative process was separately demonstrated in previous studies. Here, we investigate the interaction between Plg and epithelial TM and its effect on wound healing. Characterization of the wound margin revealed that Plg and TM were simultaneously upregulated at the early stage of wound healing and the two molecules were bound together. In vitro, TM silencing or knockout in keratinocytes inhibited Plg activation. Plg treatment enhanced keratinocyte proliferation and migration, and these actions were abolished by TM antibody. Keratinocyte-expressed vascular endothelial growth factor (VEGF), which presented a dose-response relationship with Plg treatment, can be suppressed by TM silencing. Moreover, treatment with VEGF antibody inhibited Plg-enhanced keratinocyte proliferation and wound recovery. In vivo, TM antibody treatment and keratinocyte-specific TM knockout can impede Plg-enhanced wound healing in mice. In high-glucose environments, Plg-enhanced VEGF expression and wound healing were suppressed due at least in part to downregulation of keratinocyte-expressed TM. Taken together, our findings suggest that activation of Plg/TM signaling may hold therapeutic potential for chronic wounds in diabetic or non-diabetic individuals.Key messagesPlg binds to TM in cutaneous wound healing.TM facilitates the activation of Plg to Plm in keratinocytes.Epithelial TM regulates Plg-enhanced wound healing through VEGF expression.
    link: http://dx.doi.org/10.1007/s00109-018-1702-1
    Appears in Collections:[觀光事業管理系(含溫泉所)] 期刊論文

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