Scar and fibrosis are the end result of tissue injury and disease. They are a major health problem because scarring does not replace lost function at the site of tissue injury, and no proven therapy for scarring exists. Remarkably, fetal full-thickness skin wounds heal with restoration of normal epidermal and dermal architecture. The central hypothesis to be tested in this proposal is that the biology of scarless wound healing can be differentiated from the biology of scar formation by altered genomic expression responses.
Specific Aim (1): to perform genome-wide expression analysis of fetal and adult skin, and fetal (scarless) and adult (scarring) wounds.
Specific Aim (2): to confirm array data with northern analysis and localize biologically relevant cDNAs for analysis. The goal of this research is to identify genes that are differentially regulated during scarless versus scarring wound healing. We hypothesize these genes can be used to modulate the biology of adult wound healing. This first step will form our basis for developing treatment to induce scarless healing.
