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Titolo:
TRANSFORMING GROWTH-FACTOR-BETA-1 MODULATES BETA-1 AND BETA-5 INTEGRIN RECEPTORS AND INDUCES THE DE-NOVO EXPRESSION OF THE ALPHA-V-BETA-6 HETERODIMER IN NORMAL HUMAN KERATINOCYTES - IMPLICATIONS FOR WOUND-HEALING
Autore:
ZAMBRUNO G; MARCHISIO PC; MARCONI A; VASCHIERI C; MELCHIORI A; GIANNETTI A; DELUCA M;
Indirizzi:
CTR BIOTECHNOL AVANZATE,EPITHELIAL BIOL & BIOTECHNOL UNIT,IST,NATL CANC INST I-16132 GENOA ITALY CTR BIOTECHNOL AVANZATE,EPITHELIAL BIOL & BIOTECHNOL UNIT,IST,NATL CANC INST I-16132 GENOA ITALY IST SCI SAN RAFFAELE,DIBIT,DEPT BIOL & TECHNOL RES I-20132 MILAN ITALY IST DERMOPATICO IMMACOLATA ROME ITALY UNIV MODENA,DEPT DERMATOL I-41100 MODENA ITALY
Titolo Testata:
The Journal of cell biology
fascicolo: 3, volume: 129, anno: 1995,
pagine: 853 - 865
SICI:
0021-9525(1995)129:3<853:TGMBAB>2.0.ZU;2-E
Fonte:
ISI
Lingua:
ENG
Soggetto:
HUMAN EPIDERMAL-KERATINOCYTES; CULTURED HUMAN KERATINOCYTES; SQUAMOUS-CELL CARCINOMAS; EPITHELIAL-CELLS; TISSUE-REPAIR; DIFFERENTIAL EXPRESSION; FIBRONECTIN RECEPTOR; REGULATES EXPRESSION; BM-600 NICEIN; BURN WOUNDS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
94
Recensione:
Indirizzi per estratti:
Citazione:
G. Zambruno et al., "TRANSFORMING GROWTH-FACTOR-BETA-1 MODULATES BETA-1 AND BETA-5 INTEGRIN RECEPTORS AND INDUCES THE DE-NOVO EXPRESSION OF THE ALPHA-V-BETA-6 HETERODIMER IN NORMAL HUMAN KERATINOCYTES - IMPLICATIONS FOR WOUND-HEALING", The Journal of cell biology, 129(3), 1995, pp. 853-865

Abstract

The molecular mechanism underlying the promotion of wound healing by TGF-beta 1 is incompletely understood. We report that TGF-beta 1 regulates the regenerative/migratory phenotype of normal human keratinocytes by modulating their integrin receptor repertoire. In growing keratinocyte colonies but not in fully stratified cultured epidermis, TGF-beta 1: (a) strongly upregulates the expression of the fibronectin receptor alpha 5 beta 1, the vitronectin receptor alpha v beta 5, and the collagen receptor alpha 2 beta 1 by differentially modulating the synthesis of their alpha and beta subunits; (b) downregulates the multifunctional alpha 3 beta 1 heterodimer; (c) induces the de novo expression and surface exposure of the alpha v beta 6 fibronectin receptor; (d) stimulates keratinocyte migration toward fibronectin and vitronectin; (e) induces a marked perturbation of the general mechanism of polarized domain sorting of both beta 1 and beta 4 dimers; and (f) causes a pericellular redistribution of alpha v beta 5. These data suggest that alpha 5 beta 1, alpha v beta 6, and alpha v beta 5, not routinely used bykeratinocytes resting on an intact basement membrane, act as ''emergency'' receptors, and uncover at least one of the molecular mechanisms responsible for the peculiar integrin expression in healing human wounds. Indeed, TGF-beta 1 reproduces the integrin expression pattern of keratinocytes located at the injury site, particularly of cells in the migrating epithelial tongue at the leading edge of the wound. Since these keratinocytes are inhibited in their proliferative capacity, thesedata might account for the apparent paradox of a TGF-beta 1-dependentstimulation of epidermal wound healing associated with a growth inhibitory effect on epithelial cells.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 15/07/20 alle ore 20:08:33