July 16, 2019

A critical factor for wound healing

Vanderbilt-Ingram Cancer Center scientists have discovered a role for a tumor suppressor protein in skin wound healing.

The p53 family of transcription factors (p63 and p73) plays critical roles in keratinocyte (skin cell) function.

Using mouse skin as a model system, J. Scott Beeler, Jennifer Pietenpol, PhD, and colleagues found that p73 is required for the timely healing of cutaneous wounds. In normal tissue, p73 expression increased in response to wounding, whereas p73 deficiency resulted in delayed wound healing, they reported in the journal PLOS ONE.

The delay in healing in p73-deficient mice was accompanied by increased levels of biomarkers of the DNA damage response in basal keratinocytes at the epidermal wound edge. They also found that p73 was expressed by epidermal and hair follicle stem cells, which are required for wound healing.

Further, they discovered that p73 isoforms expressed in the skin enhance p63-mediated expression of keratinocyte genes during cellular reprogramming from a mesenchymal to basal keratinocyte-like cell.

The study establishes a role for p73 in cutaneous wound healing through regulation of basal keratinocyte function.

This research was supported by the National Institutes of Health (grants CA105436, CA070856, CA098131, CA068485, GM007347).