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Titolo:
Glucose potentiates interleukin-1 beta (IL-1 beta)-induced p38 mitogen-activated protein kinase activity in rat pancreatic islets of Langerhans
Autore:
Sprinkel, AME; Andersen, NA; Mandrup-Poulsen, T;
Indirizzi:
Steno Diabet Ctr, DK-2820 Gentofte, Denmark Steno Diabet Ctr Gentofte Denmark DK-2820 Ctr, DK-2820 Gentofte, Denmark
Titolo Testata:
EUROPEAN CYTOKINE NETWORK
fascicolo: 2, volume: 12, anno: 2001,
pagine: 331 - 339
SICI:
1148-5493(200104/06)12:2<331:GPIB(B>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE PRODUCTION; NECROSIS-FACTOR-ALPHA; SECRETING BETA-CELLS; NF-KAPPA-B; INSULIN-SECRETION; GENE-EXPRESSION; SIGNAL-TRANSDUCTION; INTERFERON-GAMMA; IN-VITRO; CERAMIDE;
Keywords:
interleukin-1 beta; p38; ERK1/2; JNK; nitric oxide; diabetes mellitus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
49
Recensione:
Indirizzi per estratti:
Indirizzo: Mandrup-Poulsen, T Steno Diabet Ctr, 2 Niels Steensens Vej, DK-2820 Gentofte, Denmark Steno Diabet Ctr 2 Niels Steensens Vej Gentofte Denmark DK-2820
Citazione:
A.M.E. Sprinkel et al., "Glucose potentiates interleukin-1 beta (IL-1 beta)-induced p38 mitogen-activated protein kinase activity in rat pancreatic islets of Langerhans", EUR CYTOKIN, 12(2), 2001, pp. 331-339

Abstract

The cytokine interleukin-1 beta (IL-1 beta) is cytotoxic to rat pancreaticbeta -cells and has been implicated in the pathogenesis of insulin-dependent diabetes mellitus. IL-1 beta causes expression of inducible nitric oxidesynthase (iNOS) and production of nitric oxide (NO). NO may be the mediator of the cytotoxic effect of IL-1 beta in rat islets and beta -cell lines. Glucose has been shown to modulate the effects of IL-1 beta on accumulated insulin release and potentiate NO production in rat islets, but the biochemical mechanism is unknown. IL-1 beta activates the mitogen-activated protein kinases (MAPK) extracellular signal-regulated kinase 1 and 2 (ERK1/2), p38 and c-jun NH2-terminal kinase (JNK) in rat islets and beta -cells. Glucose may modulate MAPK activity although contrasting data have been published. The aim of this study was to investigate whether glucose potentiated IL-1 beta -induced p38 and ERK1/2 activity in rat islets. It was shown that glucose alone increased the phosphorylation of the MAPK substrates Elk-l and activating transcription factor 2 (ATF2). D-glucose potentiated the p38 activity induced by a low concentration of IL-1 beta, whereas no effect was seenat high concentrations of IL-1 beta. Inhibition of p38 activity prevented IL-1 beta -induced nitrite production in the presence of D-glucose. We conclude that IL-1 beta -induced NO production in the presence of glucose is signalled by the p38 pathway.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/04/20 alle ore 15:02:17