TITLE:
Wound Closure on the Neonatal Rat Skin I. The Modulation of the Thickness of Epidermis at the Closing Incisional Wounds
AUTHORS:
Mary Arai, Takashi Matsuzaki, Setsunosuke Ihara
KEYWORDS:
Wound Healing; Reepithelialization; Rat; Neonate; Epidermis; Terminal Differentiation; Cornification
JOURNAL NAME:
CellBio,
Vol.2 No.4,
December
20,
2013
ABSTRACT:
Full-thickness incisional wounds were made on the dorsal
skin of 1-day-old rats to elucidate the mechanism of the fluctuation
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 undergoing 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 keratinocytes may coordinately cause the fluctuation
of the thickness of the epidermis at the wound site in rat neonates.