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Titolo:
LPS induces apoptosis in macrophages mostly through the autocrine production of TNF-alpha
Autore:
Xaus, J; Comalada, M; Valledor, AF; Lloberas, J; Lopez-Soriano, F; Argiles, JM; Bogdan, C; Celada, A;
Indirizzi:
Univ Barcelona, Fac Biol, Dept Fisiol, E-08028 Barcelona, Spain Univ Barcelona Barcelona Spain E-08028 Fisiol, E-08028 Barcelona, Spain Univ Barcelona, Fac Biol, Fdn August Pi I Sunyer, E-08028 Barcelona, SpainUniv Barcelona Barcelona Spain E-08028 Sunyer, E-08028 Barcelona, Spain Univ Barcelona, Fac Biol, Dept Bioquim & Biol Mol, E-08028 Barcelona, Spain Univ Barcelona Barcelona Spain E-08028 iol Mol, E-08028 Barcelona, Spain Univ Erlangen Nurnberg, Inst Klin Mikrobiol Immunol & Hyg, Erlangen, Germany Univ Erlangen Nurnberg Erlangen Germany mmunol & Hyg, Erlangen, Germany
Titolo Testata:
BLOOD
fascicolo: 12, volume: 95, anno: 2000,
pagine: 3823 - 3831
SICI:
0006-4971(20000615)95:12<3823:LIAIMM>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; INDUCED CELL-DEATH; MONOMETHYL-L-ARGININE; NF-KAPPA-B; SEPTIC SHOCK; MEDIATED APOPTOSIS; BACTERIAL-INFECTION; SIGNALING PATHWAYS; MURINE MACROPHAGES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
78
Recensione:
Indirizzi per estratti:
Indirizzo: Celada, A Univ Barcelona, Fac Biol, Dept Fisiol, Av Diagonal 645, E-08028 Barcelona,Spain Univ Barcelona Av Diagonal 645 Barcelona Spain E-08028 na,Spain
Citazione:
J. Xaus et al., "LPS induces apoptosis in macrophages mostly through the autocrine production of TNF-alpha", BLOOD, 95(12), 2000, pp. 3823-3831

Abstract

The deleterious effects of lipopolysaccharide (LPS) during endotoxic shockare associated with the secretion of tumor necrosis factor (TNF) and the production of nitric oxide (NO), both predominantly released by tissue macrophages. We analyzed the mechanism by which LPS induces apoptosis in bone marrow-derived macrophages (BMDM), LPS-induced apoptosis reached a plateau atabout 6 hours of stimulation, whereas the production of NO by the inducible NO-synthase (iNOS) required between 12 and 24 hours. Furthermore, LPS-induced early apoptosis was only moderately reduced in the presence of an inhibitor of iNOS or when using macrophages from iNOS -/-mice, In contrast, early apoptosis was paralleled by the rapid secretion of TNF and was almost absent in macrophages from mice deficient for one (p55) or both (p55 and p75)TNF-receptors, During the late phase of apoptosis (12-24 hours) NO significantly contributed to the death of macrophages even in the absence of TNF-receptor signaling. NO-mediated cell death, but not apoptosis induced by TNF, correlated with the induction of p53 and Bar genes. Thus, LPS-induced apoptosis results from 2 independent mechanisms: first and predominantly, through the autocrine secretion of TNF-alpha (early apoptotic events), and second, through the production of NO (late phase of apoptosis). (C) 2000 by TheAmerican Society of Hematology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 09/07/20 alle ore 13:28:58