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KGF-2 Regulates STAP-2-Mediated Signal Transducer and Activator of Transcription 3 Signaling and Reduces Skin Scar
Qingde Zhou1, Jianxiang Gong2, Jianing Bi2
1Department of Dermatology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, China; Laboratory of Zhejiang Province for Pharmaceutical Engineering and Development of Growth Factors, Collaborative Biomedical Innovation Center of Wenzhou, Wenzhou, China.
Abstract:
Hypertrophic scar is a common complication of burns, skin trauma, and postoperative trauma, which involves excessive proliferation of fibroblasts and accumulation of a large amount of disorganized collagen fibers and extracellular matrix. KGF-2 plays important roles in the regulation of cellular homeostasis and wound healing. In this study, we investigated the effect and underlying mechanism of KGF-2 on scar formation after wound healing both in vitro and in vivo. We show that KGF-2 attenuates mechanical stress-induced scar formation while promoting wound healing. Mechanistically, KGF-2 inhibits STAP-2 expression and signal transducer and activator of transcription 3 activation, leading to significantly reduced collagen I and collagen III levels. Our results provide an insight into the role of KGF-2 in wound healing and scar formation and the therapeutic potential for reducing scarring while promoting wound healing.
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