| Summary: | 博士 === 國立成功大學 === 基礎醫學研究所 === 102 === Dermal fibroblasts/myofibroblasts involves in the wound healing and secretes growth factors and chemoattractants to create new substrates and proteins in the extracellular matrix (ECM). Activation of fibroblasts plays a key role in the wound healing and injury repair. Galectin-1(Gal-1) is a β - galactose - binding lectins and involves in many physiological functions, such as apoptosis, proliferation, invasion and metastasis. We have indicated that Gal-1 induced up-regulation of α-SMA, a marker of myofibroblasts, in human gingival fibroblasts (HGFs). However, the mechanism of Gal-1 induced myofibroblast activation was still unclear. In vitro study, we found that Gal-1 played an inducer in myofibroblast activation, migration and proliferation by triggering cellular reactive oxygen species (ROS) production. NADPH oxidase 4 (NOX4, a ROS producing protein) was up-regulated in Gal-1-induced myofibroblast activation. Similar to TGF-β1-induced myofibroblast activation, Gal-1 stimulated phosphorylation of Smad3 which was the upstream of NOX4. Moreover, Gal-1 induced Smad3/NOX4 pathway though Neuropilin-1/TGFBR1 in myofibroblast activation. In vivo study, Gal-1 also turned on the Smad3/NOX4 pathway during dermal myofibroblast activation and dermal wound healing. To be a clinical approach in the future, we made several cutaneous wounds per mouse and subcutaneously injected purified Gal-1 on the wound areas as animal experiments. As expected, Gal-1 accelerated general and pathological (STZ-induced diabetes mellitus) wounds healing. Taken together, Gal-1 may be a potential therapeutic target in pathological or imperfect wound healing.
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