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Titolo:
Gangliosides activate cultured bat brain microglia
Autore:
Pyo, H; Joe, EH; Jung, S; Lee, SH; Jou, I;
Indirizzi:
Ajou Univ, Sch Med, Dept Pharmacol, Suwon 442749, South Korea Ajou Univ Suwon South Korea 442749 Pharmacol, Suwon 442749, South Korea Ajou Univ, Sch Med, Dept Physiol, Suwon 442749, South Korea Ajou Univ Suwon South Korea 442749 pt Physiol, Suwon 442749, South Korea
Titolo Testata:
JOURNAL OF BIOLOGICAL CHEMISTRY
fascicolo: 49, volume: 274, anno: 1999,
pagine: 34584 - 34589
SICI:
0021-9258(199912)274:49<34584:GACBBM>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
FACTOR-KAPPA-B; HUMAN NEUROBLASTOMA-CELLS; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; GROWTH-FACTOR RECEPTOR; NITRIC-OXIDE SYNTHASE; PERITONEAL-MACROPHAGES; CEREBROSPINAL-FLUID; CYTOKINE PRODUCTION; INTERFERON-GAMMA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Joe, EH San 5 Woncheon Dong,Paldal Gu, Suwon 442749, South Korea San 5 Woncheon Dong,Paldal Gu Suwon South Korea 442749 uth Korea
Citazione:
H. Pyo et al., "Gangliosides activate cultured bat brain microglia", J BIOL CHEM, 274(49), 1999, pp. 34584-34589

Abstract

Microglia, brain resident macrophages, are activated in brain injuries andseveral neurodegenerative diseases. However, microglial activators that are produced in the brain are not yet defined. In this study, we showed that gangliosides, sialic acid-containing glycosphingolipids, could be a microglial activator. Gangliosides induced production of nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) and expression of cyclooxygenase-a (COX-2). The effect of gangliosides on NO release increased dose-dependently in the range of 10-100 mu g/ml; however, the effect decreased at concentrations higher than 200 mu g/ml. Specific types of gangliosides showed differential effects on microglial activation. Similar to gangliosides, GT1b induced production of NO and TNF-alpha and expression of COX-2. However, GM1 and GD1a induced expression of COX-2 but had little effect on NO and TNF-alpha release. The effect of gangliosides and GT1b an NO release was reduced in the presence of neuraminidase, which removes sialic acid residues from gangliosides and GT1b. Gangliosides activated extracellular signal-regulated kinase significantly but activated c-jun N-terminal kinase/stress-activated protein kinase and p38 relatively weakly. The inhibition of extracellular signal-regulated kinase by PD98059 reduced NO release from both gangliosides- and GT1b-treated microglia whereas inhibition of p38 by SB203580 increased it rather slightly. Gangliosides activated NF-kappa B, and N-acetyl cystein, an inhibitor of NF-kappa B, reduced NO release. These results suggest that gangliosides could be a microglial activator that functions via activation of mitogen-activated protein kinase and NF-kappa B.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/09/20 alle ore 13:28:04