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Titolo:
Mice lacking desmocollin 1 show epidermal fragility accompanied by barrierdefects and abnormal differentiation
Autore:
Chidgey, M; Brakebusch, C; Gustafsson, E; Cruchley, A; Hail, C; Kirk, S; Merritt, A; North, A; Tselepis, C; Hewitt, J; Byrne, C; Fassler, R; Garrod, D;
Indirizzi:
Univ Manchester, Sch Biol Sci, Manchester M13 9PT, Lancs, England Univ Manchester Manchester Lancs England M13 9PT M13 9PT, Lancs, England Univ Birmingham, Div Med Sci, Birmingham B15 2TH, W Midlands, England UnivBirmingham Birmingham W Midlands England B15 2TH W Midlands, England Lund Univ, Dept Expt Pathol, S-22185 Lund, Sweden Lund Univ Lund Sweden S-22185 iv, Dept Expt Pathol, S-22185 Lund, Sweden Barts & London Queen Marys Sch Med & Dent, London E1 2AT, England Barts & London Queen Marys Sch Med & Dent London England E1 2AT England Max Planck Inst Biochem, Dept Mol Med, D-82152 Martinsried, Germany Max Planck Inst Biochem Martinsried Germany D-82152 Martinsried, Germany
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 5, volume: 155, anno: 2001,
pagine: 821 - 832
SICI:
0021-9525(20011126)155:5<821:MLD1SE>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; DESMOSOMAL CADHERINS; MONOCLONAL-ANTIBODY; PEMPHIGUS FOLIACEUS; CELL PROLIFERATION; CORNIFIED ENVELOPE; CORNEAL EPITHELIUM; SKIN DEVELOPMENT; TRANSGENIC MICE; DEFICIENT MICE;
Keywords:
desmosome; desmocollin; epidermis; epidermal barrier; null mutation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Garrod, D Univ Manchester, Sch Biol Sci, 3-239 Stopford Bldg,Oxford Rd, Manchester M13 9PT, Lancs, England Univ Manchester 3-239 Stopford Bldg,OxfordRd Manchester Lancs England M13 9PT
Citazione:
M. Chidgey et al., "Mice lacking desmocollin 1 show epidermal fragility accompanied by barrierdefects and abnormal differentiation", J CELL BIOL, 155(5), 2001, pp. 821-832

Abstract

The desmosomal cadherin desmocollin (Dsc)1 is expressed in upper epidermiswhere strong adhesion is required. To investigate its role in vivo, we have genetically engineered mice with a targeted disruption in the Dsc1 gene. Soon after birth, null mice exhibit flaky skin and a striking punctate epidermal barrier defect. The epidermis is fragile, and acantholysis in the granular layer generates localized lesions, compromising skin barrier function. Neutrophils accumulate in the lesions and further degrade the tissue, causing sloughing (flaking) of lesional epidermis, but rapid wound healing prevents the formation of overt lesions. Null epidermis is hyperproliferative and overexpresses keratins 6 and 16, indicating abnormal differentiation. From 6 wk, null mice develop ulcerating lesions resembling chronic dermatitis. We speculate that ulceration occurs after acantholysis in the fragile epidermis because environmental insults are more stringent and wound healing is less rapid than in neonatal mice. This dermatitis is accompanied by localized hair loss associated with formation of utriculi and dermal cysts, denoting hair follicle degeneration. Possible resemblance of the lesions to human blistering diseases is discussed. These results show that Dsc1 is required for strong adhesion and barrier maintenance in epidermis and contributes to epidermal differentiation.

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Documento generato il 29/09/20 alle ore 00:46:02