Abstract
The molecular clock is coordinated by the genes BMAL1, PER1, PER2, PER3, CRY1, and CRY2, which control essential organ functions, such as the cicatrization of the skin. We aimed to determine whether the PER2 gene has an impact on skin healing. Two groups (wild-type [WT] and knockout for the PER2 gene) with 9 male mice each, were anesthetized by inhalation, and 2, 6-mm wounds were created in their dorsal skin trough with a punch biopsy instrument. A silicone ring was sutured around the perimeter of injury to restrict contraction. The wound healing was measured daily until complete healing (index of closure). In addition, quantification of the BrdU antibody was performed by subcutaneous injection technique 1 hour before euthanasia and immunochemistry. Statistically significant differences were observed in the healing time between the WT mice (who showed healing in 15.5 days) and PER2 gene mice (who showed healing in 13.5 days; P = .001). Regarding the immunoexpres- sion of BrdU, a greater expression of PER2 was observed in the normal epithelium of animals (P = .01), and this difference was decreased in wound site (P = .03). The healing assay demonstrated that the absence of the PER2 gene positively impacts the healing time of the skin in vivo, and this acceleration may be related in part to the proliferative capacity of genetically modified animals.
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