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Titolo:
DUCTUS-ARTERIOSUS SMOOTH-MUSCLE CELL-MIGRATION ON COLLAGEN - DEPENDENCE ON LAMININ AND ITS RECEPTORS
Autore:
CLYMAN RI; TANNENBAUM J; CHEN YQ; COOPER D; YURCHENCO PD; KRAMER RH; WALEH NS;
Indirizzi:
UNIV CALIF SAN FRANCISCO,CARDIOVASC RES INST SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT PEDIAT SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT ANAT SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT STOMATOL SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,LANGLEY PORTER INST SAN FRANCISCO CA 94143 RUTGERS STATE UNIV,ROBERT WOOD JOHNSON MED SCH PISCATAWAY NJ 08854
Titolo Testata:
Journal of Cell Science
, volume: 107, anno: 1994,
parte:, 4
pagine: 1007 - 1018
SICI:
0021-9533(1994)107:<1007:DSCOC->2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
LAMININ-NIDOGEN COMPLEX; EXTRACELLULAR-MATRIX; BINDING-SITE; A-CHAIN; NEURITE OUTGROWTH; INTEGRIN RECEPTOR; ENDOTHELIAL-CELLS; FRAGMENT E8; SHORT ARMS; ADHESION;
Keywords:
FIBRONECTIN; CELL MIGRATION; COLLAGEN; VASCULAR SMOOTH MUSCLE; INTEGRIN; ADHESION; ANTIADHESION; HEPARIN; LAMININ;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
60
Recensione:
Indirizzi per estratti:
Citazione:
R.I. Clyman et al., "DUCTUS-ARTERIOSUS SMOOTH-MUSCLE CELL-MIGRATION ON COLLAGEN - DEPENDENCE ON LAMININ AND ITS RECEPTORS", Journal of Cell Science, 107, 1994, pp. 1007-1018

Abstract

During permanent closure of the ductus arteriosus, smooth muscle cells migrate through the extracellular matrix (ECM) to form intimal mounds that occlude the vessel's lumen. Smooth muscle cells (SMC) migrate over surfaces coated with collagen in vitro. During the migration SMC also synthesize fibronectin (FN) and laminin (LN). Antibodies against FN and LN inhibit migration on collagen by 30% and 67%, respectively. Because of the apparent importance of LN in migration, we examined how SMC interact with LN and LN fragments (P1, E8, P1', E1', E3, E4, and G). Ductus SMC adhere to high concentrations of LN and to two fragmentsof the molecule: P1 and Eg. They use a unique set of integrin receptors to bind to LN (alpha(1) beta(1), alpha(6) beta(1) and alpha(v) beta(3)), to P1 (alpha(1) beta(1), alpha(v) beta(3)), and to E8 (alpha(6) beta(1), (alpha(v) beta(3)). The alpha(v) beta(3) integrin binds to the pi fragment of LN in an RGD peptide-dependent manner, and to the E8 fragment in an RGD-independent manner; the RGD site on the P1 fragmentprobably is not available to the cell in intact LN. Antibodies against beta(1) integrins completely inhibit SMC adhesion to LN; antibodies against the alpha(v) beta(3) integrin do not block SMC adhesion to LN,but do prevent cell spreading. LN is also capable of interfering withSMC adhesion to other ECM components. The antiadhesive effect of LN is located in the E1' domain. Both exogenous and endogenous LN increaseSMC motility on collagen I. The locomotion-promoting activity of LN resides in the Ell antiadhesive domain, and not in its adhesive (Pi, E8) domains. LN causes a decrease in the number of focal contacts on collagen I. This might enable SMC to alter their mobility as they move through the extracellular matrix to occlude the ductus arteriosus lumen.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 24/11/20 alle ore 13:15:26