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Re-epithelialization rate and protein expression in the suction-induced wound model: comparison between intact blisters, open wounds and calcipotriol-pretreated open wounds

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We have investigated re-epithelialization following induction of suction blisters in humans in intact blisters, open wounds, i.e. blister roofs removed immediately after blister induction, and calcipotriol-pretreated open wounds. Intact blisters simulate blister healing in bullous disease, while open wounds simulate re-epithelialization during wound healing. Re-epithelialization was clearly faster in open wounds than in intact blisters, and was not affected by calcipotriol pretreatment. Bullous pemphigoid antigen 2 (BP180), bullous pemphigoid antigen 1 (BP230), plectin/hemidesmosomal 1 protein (HD1), laminin 5, laminin α5, laminin β1, type VII collagen, tenascin-C, β4, αvβ5, α5 and α9 integrins were studied in intact blisters and open wounds by immunohistochemistry. Hemidesmosomal plaque proteins BP230 and plectin/HD1, which connect the keratin cytoskeleton to the hemidesmosome, appeared earlier at the leading edge in intact blisters than in open wounds. Band-like immunostaining in the basement membrane for laminin 5, α5 and β1 chains was continuous in blister bases, but partially discontinuous in open wound bases. The other antigens studied showed similar expression in intact blisters and open wounds. BP180, BP230, plectin/HD1, β4 integrin, laminin 5 and tenascin-C expression were further studied in calcipotriol-pretreated open wounds. Calcipotriol did not affect the expression of these antigens. The immunohistochemical results suggest that the keratin cytoskeleton is linked to the basal plasma membrane of migrating basal cells via BP230 and plectin/HD1 earlier in the more slowly re-epithelializing blisters than in open wounds. An intact laminin sheath may inhibit keratinocyte migration in intact blisters.
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Keywords: calcipotriol; hemidesmosome; integrin; laminin; suction blister; wound healing

Document Type: Research Article

Affiliations: 1: Department of Dermatology, Central Military Hospital, Helsinki, Finland 2: Department of Dentistry, University of Helsinki, Finland 3: Nagoya University, School of Informatics and Sciences/Graduate School of Human Informatics, Biological Systems, Chikusa-ku, Nagoya 464-01, Japan 4: Cutaneous Biology Research Center, Harvard Medical School, Massachusetts General Hospital E, Bldg 149, 13th St, Charlestown, MA 02129, U.S.A. 5: Department of Anatomy, Institute of Biomedicine, PO Box 9, FIN-00014 University of Helsinki, Helsinki, Finland 6: Department of Dermatology, Oulu University Hospital and University of Oulu, Oulu, Finland

Publication date: May 1, 2000

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