Selective modulation of BV-2 microglial activation by prostaglandin E(2). Differential effects on endotoxin-stimulated cytokine induction.

Détails

ID Serval
serval:BIB_BD9A8228E83B
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Selective modulation of BV-2 microglial activation by prostaglandin E(2). Differential effects on endotoxin-stimulated cytokine induction.
Périodique
Journal of Biological Chemistry
Auteur(s)
Petrova T.V., Akama K.T., Van Eldik L.J.
ISSN
0021-9258 (Print)
ISSN-L
0021-9258
Statut éditorial
Publié
Date de publication
1999
Volume
274
Numéro
40
Pages
28823-28827
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.Publication Status: ppublish
Résumé
The influence of prostaglandins on glial functions and, more specifically, on glial activation is not well understood. We report here that prostaglandin E(2) (PGE(2)), one of the major prostaglandins produced in the brain, acts as a potent and selective inhibitor of tumor necrosis factor alpha (TNF-alpha) production in lipopolysaccharide-stimulated primary microglia and the microglial cell line BV-2. The IC(50) for this effect is 1 nM, and 100 nM PGE(2) suppresses TNF-alpha production by >95%. More detailed studies of BV-2 cells show that PGE(2) also prevents the secretion of interleukin (IL)-6 but does not significantly modify lipopolysaccharide-stimulated expression of cyclooxygenase-2, pro-IL-1beta, or inducible nitric oxide synthase. PGE(2) appears to act primarily at the level of translation or protein stability, because TNF-alpha and IL-6 mRNA levels were only modestly decreased at high PGE(2) concentrations; concomitantly with this inhibition, PGE(2) up-regulated the levels of IL-1beta mRNA. The effects of PGE(2) could be largely mimicked by 8-bromo-cAMP, suggesting that, as in other cell types, PGE(2) action is mediated at least in part by a rise in intracellular cyclic AMP. However, the protein kinase A inhibitor H89 only partially reversed the inhibition of TNF-alpha production by PGE(2), implying that the PGE(2) effect in BV-2 cells is mediated through both protein kinase A-dependent and -independent pathways.
Mots-clé
Animals, Base Sequence, Cell Line, Cyclic AMP/metabolism, Cyclic AMP-Dependent Protein Kinases/metabolism, DNA Primers, Dinoprostone/pharmacology, Endotoxins/pharmacology, Interleukin-1/biosynthesis, Interleukin-1/genetics, Interleukin-6/biosynthesis, Interleukin-6/genetics, Mice, Microglia/drug effects, Microglia/metabolism, RNA, Messenger/genetics, RNA, Messenger/metabolism, Rats, Tumor Necrosis Factor-alpha/biosynthesis, Tumor Necrosis Factor-alpha/genetics
Pubmed
Web of science
Création de la notice
30/01/2014 17:28
Dernière modification de la notice
03/03/2018 20:59
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