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  • Title: Exosomes from adipose-derived mesenchymal stem cell improve diabetic wound healing and inhibit fibrosis via miR-128-1-5p/TGF-β1/Smad axis.
    Author: Liang Q, Zhou D, Ge X, Song P, Chu W, Xu J, Shen Y.
    Journal: Mol Cell Endocrinol; 2024 Jul 01; 588():112213. PubMed ID: 38556162.
    Abstract:
    OBJECTIVE: Difficult-to-heal wound is a prevalent and significant complication of diabetes, characterized by impaired functionality of epithelial cells such as fibroblasts. This study aims to investigate the potential mechanism of ADSC-Exos promoting diabetic wound healing by regulating fibroblast function. MATERIALS AND METHODS: ADSC-Exos were confirmed through TEM, NTA, and Western Blot techniques. The study conducted on rat skin fibroblasts (RSFs) exposed to 33 mmol/L glucose in vitro. We used cck-8, EDU, transwell, and scratch assays to verify the proliferation and migration of RSFs. Furthermore, levels of TGF-β1 and α-SMA proteins were determined by immunofluorescence and Western Blot. RSFs were transfected with miR-128-1-5p mimics and inhibitors, followed by quantification of TGF-β1, α-SMA, Col I and Smad2/3 protein levels using Western Blot. In vivo, the effects of ADSC-Exos on diabetic wounds were assessed using digital imaging, histological staining, as well as Western Blot analysis. RESULTS: In vitro, ADSC-Exos significantly enhanced proliferation and migration of RSFs while reducing the expression of TGF-β1 and α-SMA. In vivo, ADSC-Exos effectively promoted diabetic wound healing and mitigated scar fibrosis. Additionally, ADSC-Exos exhibited elevated levels of miR-128-1-5p, which targets TGF-β1, resulting in a notable reduction in TGF-β1, α-SMA, Col I and smad2/3 phosphorylation in RSFs. CONCLUSION: In conclusion, our results demonstrated that ADSC-Exos promoted diabetic wound healing, and inhibited skin fibrosis by regulating miR-128-1-5p/TGF-β1/Smad signaling pathway, which provides a promising innovative treatment for diabetic wound healing.
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