Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Inhibited neutrophil apoptosis: Proteasome dependent NF-kappa B translocation is required for TRAF-1 synthesis
Autore:
Nolan, B; Kim, R; Duffy, A; Sheth, K; De, M; Miller, C; Chari, R; Bankey, P;
Indirizzi:
Univ Massachusetts, Sch Med, Dept Surg, Worcester, MA 01655 USA Univ Massachusetts Worcester MA USA 01655 t Surg, Worcester, MA 01655 USA
Titolo Testata:
SHOCK
fascicolo: 3, volume: 14, anno: 2000,
pagine: 290 - 294
SICI:
1073-2322(200009)14:3<290:INAPDN>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
TUMOR-NECROSIS-FACTOR; SIGNAL-TRANSDUCTION PATHWAYS; ACTIVATED PROTEIN-KINASE; POLYMORPHONUCLEAR LEUKOCYTES; TYROSINE PHOSPHORYLATION; GRANULOCYTE APOPTOSIS; INJURED PATIENTS; IN-VITRO; LIPOPOLYSACCHARIDE; INDUCTION;
Keywords:
neutrophil; apoptosis; nuclear factor kappa B; 20-S ubiquitin proteasome;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
31
Recensione:
Indirizzi per estratti:
Indirizzo: Bankey, P Univ Massachusetts, Sch Med, Dept Surg, 55 Lake Ave N, Worcester, MA 01655USA Univ Massachusetts 55 Lake Ave N Worcester MA USA 01655 01655USA
Citazione:
B. Nolan et al., "Inhibited neutrophil apoptosis: Proteasome dependent NF-kappa B translocation is required for TRAF-1 synthesis", SHOCK, 14(3), 2000, pp. 290-294

Abstract

Neutrophil (PMN) apoptosis regulates local and systemic inflammation during sepsis. Tumor necrosis factor receptor-associated factors (TRAFs) have been implicated as mediators of apoptosis; however, the signaling pathways for their production in stimulated PMN are unclear. We hypothesize that NF-kappaB translocation is necessary for the induction of TRAF-1 in PMNs with prolonged survival. Neutrophils were isolated from the blood of healthy volunteers by Ficoll gradient centrifugation and red blood cell sedimentation. Neutrophil NF-kappaB was inhibited with a proteasome inhibitor, PSI-I. Cellswere treated with PSI-I (30 muM) or vehicle (DMSO 0.2%) for 50 min then incubated over an 18-h time course with LPS (10 to 1000 ng/mL), tumor necrosis factor alpha (TNF alpha) (2 to 20 ng/mL) or control media. in vitro apoptosis was quantified by propidium iodide FAGS analysis. Total cellular TRAF-1 was detected by Western blot analysis of cell lysates. Steady state TRAF-1 mRNA was detected by RPA. NF-kappaB activity was determined by Western blot analysis for nuclear p65. Means and standard errors were calculated; data were analyzed by ANOVA. Lipopolysaccharide (LPS) and TNF alpha increased PMN nuclear p65 and steady state TRAF-1 mRNA. Apoptosis was inhibited by TNF alpha and LPS at 12 and 18 h (P < 0.01). Incubation of cells in the NF-<kappa>B inhibitor PSI-I blocked LPS and TNF alpha -induced inhibition of apoptosis (P < 0.05) and the induction of both nuclear p65 and TRAF-1 mRNA. These data demonstrate that inhibition of PMN apoptosis and TRAF-1 induction by LPS and TNF<alpha> is NF-kappaB dependent.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/07/20 alle ore 01:39:10