Identification of a novel FcgammaRIII receptor that is up-regulated in fetal wound healing.

The mid-gestation fetus is able to heal skin wounds rapidly and without scarring, an ability that is lost as development proceeds. The aim of this study was to identify novel genes involved in this process. We established an ex vivo wound model from embryonic rats and showed that over 72 hours, embryonic day 17 wounds reepithelialized and closed whereas day 19 wounds did not. To investigate the molecular basis of this phenomenon we analyzed changes in gene expression using differential display polymerase chain reaction. We characterized one transcript that was strongly up-regulated in the healing response of wounded, day 17 skin. It encodes a protein of 249 amino acids with striking similarity to the human low-affinity receptor for the Fc portion of IgG (FcgammaRIII), suggesting that it is a novel member of the FcgammaR family, which we named FcgammaRIII-X. A wound-healing timecourse shows that FcgammaRIII-X was up-regulated in healing, wounded day 17 skin but not in nonhealing, wounded day 19 skin and that its up-regulation was accelerated in skin with multiple wounds. We suggest that up-regulation of FcgammaRIII-X may contribute to scarless healing of fetal skin.