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摘要:
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.
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篇名 Wound Closure on the Neonatal Rat Skin I. The Modulation of the Thickness of Epidermis at the Closing Incisional Wounds
来源期刊 细胞生物学(英文) 学科 医学
关键词 Wound Healing Reepithelialization Rat NEONATE EPIDERMIS Terminal Differentiation Cornification
年,卷(期) 2013,(4) 所属期刊栏目
研究方向 页码范围 248-256
页数 9页 分类号 R73
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Wound
Healing
Reepithelialization
Rat
NEONATE
EPIDERMIS
Terminal
Differentiation
Cornification
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细胞生物学(英文)
季刊
2325-7776
武汉市江夏区汤逊湖北路38号光谷总部空间
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71
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