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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Authors | Qingde Zhou, Jianxiang Gong, Jianing Bi, Xuanxin Yang, Li Zhang, Chao Lu, Lijia Li, Min Chen, Jianqiu Cai, Rongshuai Yang, Xiaokun Li, Zhiming Li, Xiaojie Wang |
Journal | The Journal of investigative dermatology
(J Invest Dermatol)
Vol. 142
Issue 7
Pg. 2003-2013.e5
(07 2022)
ISSN: 1523-1747 [Electronic] United States |
PMID | 34999107
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved. |
Chemical References |
- Adaptor Proteins, Signal Transducing
- FGF10 protein, human
- Fibroblast Growth Factor 10
- Phosphoproteins
- STAP2 protein, human
- STAT3 Transcription Factor
- Collagen
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Topics |
- Adaptor Proteins, Signal Transducing
(metabolism)
- Cicatrix, Hypertrophic
(pathology)
- Collagen
(metabolism)
- Fibroblast Growth Factor 10
(metabolism)
- Fibroblasts
(metabolism)
- Humans
- Phosphoproteins
(metabolism)
- STAT3 Transcription Factor
(metabolism)
- Skin
(injuries, pathology)
- Wound Healing
(physiology)
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