Wound Closure on the Neonatal Rat Skin I. The Modulation of the Thickness of Epidermis at the Closing Incisional Wounds

Full-thickness incisional wounds were made on the dorsal skin of 1-day-old rats to elucidate the mechanism of the fluc- tuation of the epidermal thickness after the wound closure. The thickness of the epidermis covering the wound reached a peak around 96 h post-wounding (PW), and became thinner thereafter. The analyses of the cell proliferation and apoptosis at the epidermal wound regions revealed that the rate of TUNEL-positive cells that displays the cells under- going apoptosis increased as the epidermis became thinner around 120 h PW. Next, immunohistochemical analyses using antibodies against keratinocyte differentiation marker proteins indicated that the delay or interruption of the spinous to granular transition from 96 to 120 h PW might result in the epidermal thickening in the wound region. Third, the region undyed with anti-caspase-14 antibody extended downward in the thickened epidermis by 96 h PW, and in turn, it became intensely and widely stained with this antibody in the thinning epidermis by 120 h PW. Taken together, it is likely that the delay and acceleration of the terminal differentiation, including cornification of the epidermal kerati- nocytes may coordinately cause the fluctuation of the thickness of the epidermis at the wound site in rat neonates.