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Titolo:
Crystal-induced neutrophil activation. VII. Involvement of Syk in the responses to monosodium urate crystals
Autore:
Desaulniers, P; Fernandes, M; Gilbert, C; Bourgoin, SG; Naccache, PH;
Indirizzi:
CHU Laval, Ctr Rech, Ctr Rech Rhumatol & Immunol, St Foy, PQ G1V 4G2, Canada CHU Laval St Foy PQ Canada G1V 4G2 & Immunol, St Foy, PQ G1V 4G2, Canada Univ Laval, Fac Med, Dept Med, Quebec City, PQ G1K 7P4, Canada Univ LavalQuebec City PQ Canada G1K 7P4 Quebec City, PQ G1K 7P4, Canada Univ Laval, Fac Med, Dept Physiol, Quebec City, PQ G1K 7P4, Canada Univ Laval Quebec City PQ Canada G1K 7P4 Quebec City, PQ G1K 7P4, Canada
Titolo Testata:
JOURNAL OF LEUKOCYTE BIOLOGY
fascicolo: 4, volume: 70, anno: 2001,
pagine: 659 - 668
SICI:
0741-5400(200110)70:4<659:CNAVIO>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
TYROSINE KINASE INHIBITOR; CELL ANTIGEN RECEPTOR; NECROSIS-FACTOR-ALPHA; FC-GAMMA RECEPTORS; SRC FAMILY KINASES; INFLAMMATORY MICROCRYSTALS; T-CELL; PHOSPHOLIPASE-D; CROSS-LINKING; SUPEROXIDE PRODUCTION;
Keywords:
tyrosine phosphorylation; phagocytosis; gout; CD32;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
75
Recensione:
Indirizzi per estratti:
Indirizzo: Naccache, PH CHU Laval, Ctr Rech, Ctr Rech Rhumatol & Immunol, 2705 Blvd Laurier,Room T1-49, St Foy, PQ G1V 4G2, Canada CHU Laval 2705 Blvd Laurier,Room T1-49 St Foy PQ Canada G1V 4G2
Citazione:
P. Desaulniers et al., "Crystal-induced neutrophil activation. VII. Involvement of Syk in the responses to monosodium urate crystals", J LEUK BIOL, 70(4), 2001, pp. 659-668

Abstract

The inflammatory response in acute gouty arthritis is in large part a result of the interaction between neutrophils and monosodium. urate (MSU) crystals. The tyrosine kinase Syk, which has been largely associated with the phagocytic response by Fe receptors and with spreading mediated by integrins,has been identified as one of the major proteins tyrosine-phosphorylated in human neutrophils upon stimulation by MSU crystals and is known to be mediated in part by the Fe receptor, CD16. This has led to the present examination of the implication of Syk in the activation pathways used by MSU crystals. The tyrosine-phosphorylation patterns induced by MSU crystals and by the ligation of CD16 were inhibited by piceatannol, which, conversely, only slightly delayed but did not diminish the peak of tyrosine phosphorylation induced by cross-linking CD32 or by the addition of fMet-Leu-Phe. Moreover,piceatannol inhibited the activity of Syk as monitored by in vitro kinase assays, by its in situ tyrosine phosphorylation, and by its activity towardexogenous substrates after stimulation by MSU crystals. We also measured the impact of piceatannol on the mobilization of calcium, the production of superoxide anions, and the activity of PLD stimulated by MSU crystals. We noted a distinct inhibition of all these responses by piceatannol. Finally, the morphological changes observed in neutrophils as characteristic of MSU crystal internalization were diminished significantly by piceatannol. The results obtained show that Syk plays a critical and central role in the signal-transduction pathways called upon by MSU crystals subsequent to their interaction with human neutrophils.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:18:13