Expression of different p63 variants in healing skin wounds suggests a role of p63 in reepithelialization and muscle repair.

Healing of skin wounds in mammals involves partial reconstruction of the dermis and coverage of the injured site by keratinocytes. The latter process is achieved by extensive migration and hyperproliferation of keratinocytes at the wound rim. Because the p53 protein family member p63 is expressed in human hyperproliferative epidermis, this study determined whether enhanced keratinocyte proliferation correlates with the expression of p63. Therefore, we investigated the temporal and spatial distribution of four major variants of the p63 transcription factor-TAp63alpha, TAp63gamma, DeltaNp63alpha and DeltaNp63gamma-during normal skin wound healing in mice. Transcripts encoding amino-terminally truncated DeltaNp63 variants were found at high levels in basal and suprabasal keratinocytes of the hyperproliferative wound epithelium. Interestingly, TAp63 variants, which include the conserved transactivation domain TA at their amino-terminus, were also expressed in wound keratinocytes as well as at the edge of the injured subcutaneous muscle panniculus carnosus. These findings suggest splice-variant specific functions of p63 in reepithelialization and muscle repair.