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Updated: Jul 6, 2026
A Mouse Fetal Skin Model of Scarless Wound Repair
Published on: January 16, 2015
Fetal wound healing using a genetically modified murine model: the contribution of P-selectin
Bindi Naik-Mathuria1, Andre N Gay, Ling Yu
1Division of Pediatric Surgery, Michael E. DeBakey Department of Surgery, Section of Leukocyte Biology, Baylor College of Medicine, Houston, TX 77030-2399, USA.
Purpose:
During early gestation, fetal wounds heal with paucity of inflammation and absent scar formation. P-selectin is an adhesion molecule that is important for leukocyte recruitment to injury sites. We used a murine fetal wound healing model to study the specific contribution of P-selectin to scarless wound repair.
Methods:
Linear excisional wounds were created on the dorsa of E15.5 and E17.5 gestation fetuses in wild-type and P-selectin (-/-) mice (term = 19 days). Wounds were harvested at various time-points after wounding and analyzed using histology and immunohistochemistry.
Results:
The E15.5 wounds in both wild-type and P-selectin (-/-) fetuses healed scarlessly and with minimal inflammation, whereas E17.5 wounds healed with fibrosis and inflammation. However, the scars of the P-selectin (-/-) wounds appeared slightly different than wild-type. There were significantly more inflammatory cells in E17.5 wild-type wounds 6 hours after injury (P < .001), but the difference was no longer significant by 24 hours. Finally, reepithelialization was slower in the E15.5 knockout wounds compared to their wild-type counterparts.
Conclusions:
Absence of P-selectin delays inflammatory cell recruitment and reepithelialization of fetal wounds; however, scar formation still occurs in late gestation wounds. The contribution of specific molecules to fetal wound healing can be elucidated using murine knockout or transgenic models.
