KGF-2 Regulates STAP-2–Mediated Signal Transducer and Activator of Transcription 3 Signaling and Reduces Skin Scar Formation

• Published in: Journal of investigative dermatology Vol. 142; no. 7; pp. 2003 - 2013.e5
• Main Authors: Zhou, Qingde, Gong, Jianxiang, Bi, Jianing, Yang, Xuanxin, Zhang, Li, Lu, Chao, Li, Lijia, Chen, Min, Cai, Jianqiu, Yang, Rongshuai, Li, Xiaokun, Li, Zhiming, Wang, Xiaojie
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-07-2022
• Subjects: α-SMA; COL; SF; FGF; STAT3; NF; HS; p-STAT3; ERK
• ISSN: 0022-202X; 1523-1747
• DOI: 10.1016/j.jid.2021.12.018

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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