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Updated: Aug 22, 2026

A Mouse Fetal Skin Model of Scarless Wound Repair
Published on: January 16, 2015
The impact of cyclooxygenase-2 mediated inflammation on scarless fetal wound healing
Traci A Wilgus1, Valerie K Bergdall, Kathleen L Tober
1Department of Pathology, The Ohio State University, Columbus, OH, USA.
Abstract:
Cyclooxygenase-2 (COX-2) and the prostaglandin products generated as a result of COX-2 activity mediate a variety of biological and pathological processes. Scarless healing occurs in fetal skin in the first and second trimesters of development. This scarless healing process is known to proceed without a significant inflammatory response, which appears to be important for the lack of scarring. Because the COX-2 pathway is an integral component of inflammation, we investigated its role in the fetal repair process using a mouse model of scarless fetal wound healing. COX-2 expression in scarless and fibrotic fetal wounds was examined. In addition, the ability of exogenous prostaglandin E(2) to alter scarless fetal healing was evaluated. The results suggest that the COX-2 pathway is involved in scar production in fetal skin and that targeting COX-2 may be useful for limiting scar formation in adult skin.
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