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Titolo:
Evidence for the involvement of phosphatidylinositol 3-kinase in fMLP-stimulated neutrophil adhesion to ICAM-1-transfected cells
Autore:
Pellegatta, F; Radaelli, A; Heltai, S; Yan, L; Chierchia, SL; Folli, F;
Indirizzi:
Ist Sci San Raffaele, Dept Cardiol, Lab Cardiovasc Pathophysiol, I-20132 Milan, Italy Ist Sci San Raffaele Milan Italy I-20132 hophysiol, I-20132 Milan, Italy Ist Sci San Raffaele, Lab Tumor Immunotherapy, I-20132 Milan, Italy Ist Sci San Raffaele Milan Italy I-20132 notherapy, I-20132 Milan, Italy Ist Sci San Raffaele, Unit Metab Dis, I-20132 Milan, Italy Ist Sci San Raffaele Milan Italy I-20132 Metab Dis, I-20132 Milan, Italy
Titolo Testata:
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
fascicolo: 6, volume: 37, anno: 2001,
pagine: 751 - 761
SICI:
0160-2446(200106)37:6<751:EFTIOP>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEUKOCYTE INTEGRIN LFA-1; PROTEIN-KINASE; T-CELLS; ACTIVATION; INHIBITOR; RECEPTOR; PHOSPHORYLATION; WORTMANNIN; ADHESIVENESS; PLATELETS;
Keywords:
phosphatidylinositol 3-kinase; beta(2)-integrins; neutrophils; intercellular adhesion molecule-1;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Pellegatta, F Ist Sci San Raffaele, Dept Cardiol, Lab Cardiovasc Pathophysiol, Via Olgettina 60, I-20132 Milan, Italy Ist Sci San Raffaele Via Olgettina 60 Milan Italy I-20132 y
Citazione:
F. Pellegatta et al., "Evidence for the involvement of phosphatidylinositol 3-kinase in fMLP-stimulated neutrophil adhesion to ICAM-1-transfected cells", J CARDIO PH, 37(6), 2001, pp. 751-761

Abstract

Phosphatidylinositol 3-kinase (PI-3K) controls important intracellular steps involved in inflammation, immunity, and cell growth. PI-3K also modulates leukocyte integrin adhesiveness. In this study we evaluated the role of PI-3K on neutrophil adhesion to intercellular adhesion molecule-1 (ICAM-1)-transfected cells. N-formyl-methionyl-leucyl-phenylalanine (fMLP)-stimulatedneutrophil adhesion was inhibited by wortmannin and LY294002, two unrelated PI-3K inhibitors, whereas phorbol myristate acetate (PMA)-induced neutrophil adhesion was not inhibited by them. After fMLP stimulation, a rapid activation of AKT and ERK was observed. However, only activation of AKT was reversed by the PI-3K inhibitors. Neutrophil expression of the beta (2)-integrins Mac-1, lymphocyte function-associated antigen-1(LFA-1), and gp150.95 was not affected by wortmannin, nor was expression of the activation epitoperecognized by MAB24. We conclude that (a) PI-3K is involved in fMLP-activated neutrophil adhesion to ICAM-1-transfected cells, (b) the mechanism involved is not mediated by the modulation of beta (2)-integrin expression or activation, and (c) another mechanism seems to involve the adhesion to ICAM-1 when a cellular system of adhesion is used.

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Documento generato il 18/09/20 alle ore 17:13:47