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Titolo:
Acetylcholine prevents intercellular adhesion molecule 1 (CD54)-induced focal adhesion complex assembly in endothelial cells via a nitric oxide-cGMP-dependent pathway
Autore:
Clancy, RM; Abramson, SB;
Indirizzi:
Hosp Joint Dis, Dept Rheumatol, New York, NY 10003 USA Hosp Joint Dis NewYork NY USA 10003 pt Rheumatol, New York, NY 10003 USA NYU, Sch Med, Dept Med, New York, NY USA NYU New York NY USANYU, Sch Med, Dept Med, New York, NY USA
Titolo Testata:
ARTHRITIS AND RHEUMATISM
fascicolo: 10, volume: 43, anno: 2000,
pagine: 2260 - 2264
SICI:
0004-3591(200010)43:10<2260:APIAM1>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIN; ICAM-1; VASP; PHOSPHORYLATION; PHOSPHOPROTEIN; CYTOSKELETON; INHIBITION; SEQUENCES; RECEPTOR; MOTILITY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
19
Recensione:
Indirizzi per estratti:
Indirizzo: Clancy, RM Hosp Joint Dis, Dept Rheumatol, 301 E 17th St, New York, NY 10003 USA Hosp Joint Dis 301 E 17th St New York NY USA 10003 NY 10003 USA
Citazione:
R.M. Clancy e S.B. Abramson, "Acetylcholine prevents intercellular adhesion molecule 1 (CD54)-induced focal adhesion complex assembly in endothelial cells via a nitric oxide-cGMP-dependent pathway", ARTH RHEUM, 43(10), 2000, pp. 2260-2264

Abstract

Objective, Nitric oxide (NO) is induced by exposure of endothelial cells (EC) to acetylcholine, where it acts in a paracrine manner to relax smooth muscle and as a defensive molecule to inhibit the adhesion of leukocytes to EC, The mechanism(s) of the antiadhesive properties of constitutive NO are poorly understood. In these studies, we found that NO induced by acetylcholine exerts autocrine effects, which interfere with normal adhesion mechanisms,Methods. The function of the adhesion molecule intercellular adhesion molecule 1 (CD54) of EC was measured using latex beads coated with antibody to CD54 as a model for CD54 ligation by the leukocyte beta 2 integrin, Recruitment of filamentous actin (F-actin) and of the signaling molecule vasodilator-stimulated phosphoprotein (VASP) was measured by immunofluorescence microscopy,Results. Exposure of EC to anti;CD54 beads induced the subplasmalemmal assembly of F-actin and VASP, Acetylcholine blocked the anti-CD54 bead-inducedtranslocation of F-actin and VASP; this effect was reversed by inhibition of NO production. The NO action did not interfere with binding, but completely inhibited the assembly of the focal activation complex, which we believe is necessary for firm heterotypic adhesion between leukocyte and EC, Further studies indicated that the NO effect was due to its capacity to raise cGMP, Platelet endothelial cell adhesion molecule 1 (CD31, also implicated in leukocyte adhesion) did not mimic CD54 responses. Conclusion. These results indicate that the ligation of endothelial cell CD54 induces the assembly of subplasmalemmal F-actin and the recruitment of VASP, NO derived from constitutive nitric oxide synthase acts to disrupt these CD54-elicited endothelial cell responses. This action may protect vascular endothelium from leukocyte-mediated injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 07:00:36