Differences in cutaneous mast cells affect scar formation

Abstract

Scar formation is a potentially detrimental process of tissue restoration in adults, affecting organ form and function. During fetal development there is a stage at which skin heals without inflammation or scarring. We use a murine model of fetal wound healing in which embryonic day 15 (E15) wounds heal scarlessly and without inflammation. In contrast, fetal wounds generated on embryonic day 18 (E18) heal with inflammation and scarring. One possible mediator of this change in wound healing is the mast cell. Mast cells are resident innate immune cells involved in the initiation of inflammation. We have found that the skin of E15 fetuses has fewer total mast cells than E18 skin. Furthermore, the mast cells of E15 skin are less mature and do not degranulate in response to wounding as effectively as mast cells of E18 skin. To determine if these differences in mast cells affect wound healing we utilized mast cell‐deficient mice (KitW/Wv mice) in our model. Inflammation and scar formation in wounded E18 skin was assessed. A two fold decrease in scar width was observed in the mast cell‐deficient mice compared to wild‐type littermates. These data suggest that mast cells may play an enhancing role in scar formation. More studies are needed to determine the specific mediators and mechanisms by which mast cells promote scarring. Supported in part by the Ohio State University Department of Pathology and NIH Grant CA127109.