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Titolo:
A central role for the armadillo protein plakoglobin in the autoimmune disease pemphigus vulgaris
Autore:
Caldelari, R; de Bruin, A; Baumann, D; Suter, MM; Bierkamp, C; Balmer, V; Muller, E;
Indirizzi:
Univ Bern, Inst Anim Pathol, CH-3012 Bern, Switzerland Univ Bern Bern Switzerland CH-3012 nim Pathol, CH-3012 Bern, Switzerland Ctr Dev Biol, F-31062 Toulouse, France Ctr Dev Biol Toulouse France F-31062 Dev Biol, F-31062 Toulouse, France
Titolo Testata:
JOURNAL OF CELL BIOLOGY
fascicolo: 4, volume: 153, anno: 2001,
pagine: 823 - 834
SICI:
0021-9525(20010514)153:4<823:ACRFTA>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CELL-CELL ADHESION; BETA-CATENIN; DESMOSOMAL CADHERINS; CULTURED KERATINOCYTES; INTERMEDIATE FILAMENTS; ADHERING JUNCTIONS; EPITHELIAL-CELLS; EMBRYONIC HEART; BINDING-SITES; SKIN DISEASES;
Keywords:
catenins; desmosomes; mouse keratinocytes; epithelial differentiation; blistering disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Muller, E Univ Bern, Inst Anim Pathol, Langgass Str 122, CH-3012 Bern, Switzerland Univ Bern Langgass Str 122 Bern Switzerland CH-3012 Switzerland
Citazione:
R. Caldelari et al., "A central role for the armadillo protein plakoglobin in the autoimmune disease pemphigus vulgaris", J CELL BIOL, 153(4), 2001, pp. 823-834

Abstract

In pemphigus vulgaris (PV), autoantibody binding to desmoglein (Dsg) 3 induces loss of intercellular adhesion in skin and mucous membranes. Two hypotheses are currently favored to explain the underlying molecular mechanisms:(a) disruption of adhesion through steric hindrance, and (b) interference of desmosomal cadherin-bound antibody with intracellular events, which we speculated to involve plakoglobin. To investigate the second hypothesis we established keratinocyte cultures from plakoglobin knockout (PG(-/-)) embryos and PG(+/+) control mice. Although both cell types exhibited desmosomal cadherin-mediated adhesion during calcium-induced differentiation and bound PV immunoglobin (IgG) at their cell surface, only PG(+/+) keratinocytes responded with keratin retraction and loss of adhesion. When full-length plakoglobin was reintroduced into PG(-/-) cells, responsiveness to PV IgG was restored. Moreover, in these cells Pike in PG(+/+) keratinocytes, PV IgG binding severely affected the linear distribution of plakoglobin at the plasma membrane. Taken together, the establishment of an in vitro model using PG(+/+) and PG(-/-) keratinocytes allowed us (a) to exclude the steric hindrance only hypothesis, and (b) to demonstrate for the first time that plakoglobin plays a central role in PV, a finding that will provide a novel direction for investigations of the molecular mechanisms leading to PV, and on the function of plakoglobin in differentiating keratinocytes.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 18:46:02