Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Role of von Willebrand factor in tumour cell-induced platelet aggregation:differential regulation by NO and prostacyclin
Autore:
Jurasz, P; Stewart, MW; Radomski, A; Khadour, F; Duszyk, M; Radomski, MW;
Indirizzi:
Univ Alberta, Dept Pharmacol, Edmonton, AB T6G 2H7, Canada Univ Alberta Edmonton AB Canada T6G 2H7 col, Edmonton, AB T6G 2H7, Canada Univ Alberta, Dept Physiol, Edmonton, AB T6G 2H7, Canada Univ Alberta Edmonton AB Canada T6G 2H7 iol, Edmonton, AB T6G 2H7, Canada Thrombot Inc, Edmonton, AB, Canada Thrombot Inc Edmonton AB CanadaThrombot Inc, Edmonton, AB, Canada
Titolo Testata:
BRITISH JOURNAL OF PHARMACOLOGY
fascicolo: 5, volume: 134, anno: 2001,
pagine: 1104 - 1112
SICI:
0007-1188(200111)134:5<1104:ROVWFI>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
BERNARD-SOULIER PLATELETS; GLYCOPROTEIN IB-BETA; NITRIC-OXIDE; MEMBRANE GLYCOPROTEIN; VONWILLEBRAND-FACTOR; TYROSINE PHOSPHORYLATION; COMPARATIVE PHARMACOLOGY; CANCER; RECEPTOR; ACTIVATION;
Keywords:
HT-1080 fibrosarcoma cells; platelets; adhesion; aggregation; solid-phase von Willebrand factor; glycoprotein Ib; glycoprotein IIb/IIIa; nitric oxide; prostacyclin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Radomski, MW Univ Alberta, Dept Pharmacol, 9-50 Med Sci Bldg, Edmonton, ABT6G 2H7, Canada Univ Alberta 9-50 Med Sci Bldg Edmonton AB Canada T6G 2H7 ada
Citazione:
P. Jurasz et al., "Role of von Willebrand factor in tumour cell-induced platelet aggregation:differential regulation by NO and prostacyclin", BR J PHARM, 134(5), 2001, pp. 1104-1112

Abstract

1 We have studied the effects of a novel agonist, solid-phase von Willebrand Factor (sVWF), on tumour cell-induced platelet aggregation (TCIPA).2 Washed platelet suspensions were obtained from human blood and the effects of HT-1080 human fibrosarcoma cells and sVWF on platelets were studied using aggregometry, phase-contrast microscopy, and flow cytometry.3 Incubation of platelets with sVWF (1.2 mug ml(-1)) and HT-1080 cells (5 x 10(3) ml(-1)) resulted in a two-phased reaction characterized first by the adhesion of platelets to sVWF, then by aggregation.4 TCIPA in the presence of sVWF was inhibited by S-nitroso-glutathione (GSNO, 100 muM) and prostacyclin (PCI2, 30 nm).5 Platelet activation in the presence of tumour cells and sVWF resulted inthe decreased surface expression of platelet glycoprotein (GP)Ib and up-regulation of GPIIb/IIIa receptors.6 Pre-incubation of platelets with PGI(2) (30 nm) resulted in inhibition of sVWF-tumour cell-stimulated platelet surface expression of GPIIb/IIIa as measured by flow cytometry using antibodies directed against both non-activated and activated receptor. In contrast, GSNO (100 muM) did not affect sVWF-tumour cell-stimulated platelet surface expression of GPIIb/IIIa.7 Flow cytometry performed with PAC-1 antibodies that bind only to the activated GPIIb/IIIa revealed that GSNO (100 muM) caused inhibition of activation of GPIIb/IIIa.8 The inhibitors exerted no significant effects on TCIPA-mediated changes in GPIb.9 Thus, sVWF potentiates the platelet-aggregatory activity of HT-1080 cells and these effects appear to be mediated via up-regulation of platelet GPIIb/IIIa.10 Prostacyclin and NO inhibit TCIPA-sVWF-mediated platelet aggregation. The mechanisms of inhibition of this aggregation by PGI(2) differ from thoseof NO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 08:32:37