Source:http://linkedlifedata.com/resource/pubmed/id/17390309
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
2007-4-18
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pubmed:abstractText |
G protein-coupled receptor 84 (GPR84) is a recently discovered member of the seven transmembrane receptor superfamily whose function and regulation are unknown. Here, we report that in mice suffering from endotoxemia, microglia express GPR84 in a strong and sustained manner. This property is shared by subpopulations of peripheral macrophages and, to a much lesser extent, monocytes. The induction of GPR84 expression by endotoxin is mediated, at least in part, by proinflammatory cytokines, notably tumor necrosis factor (TNF) and interleukin-1 (IL-1), because mice lacking either one or both of these molecules have fewer GPR84-expressing cells in their cerebral cortex than wild-type mice during the early phase of endotoxemia. Moreover, when injected intracerebrally or added to microglial cultures, recombinant TNF stimulates GPR84 expression through a dexamethasone-insensitive mechanism. Finally, we show that microglia produce GPR84 not only during endotoxemia, but also during experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis. In conclusion, this study reports the identification of a new sensitive marker of microglial activation, which may play an important regulatory role in neuroimmunological processes, acting downstream to the effects of proinflammatory mediators.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Dexamethasone,
http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoids,
http://linkedlifedata.com/resource/pubmed/chemical/Gpr84 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, G-Protein-Coupled,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0894-1491
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
55
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
790-800
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pubmed:meshHeading |
pubmed-meshheading:17390309-Animals,
pubmed-meshheading:17390309-Brain,
pubmed-meshheading:17390309-Cells, Cultured,
pubmed-meshheading:17390309-Dexamethasone,
pubmed-meshheading:17390309-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:17390309-Endotoxemia,
pubmed-meshheading:17390309-Gene Expression,
pubmed-meshheading:17390309-Glucocorticoids,
pubmed-meshheading:17390309-Interleukin-1,
pubmed-meshheading:17390309-Lipopolysaccharides,
pubmed-meshheading:17390309-Mice,
pubmed-meshheading:17390309-Mice, Inbred C57BL,
pubmed-meshheading:17390309-Microglia,
pubmed-meshheading:17390309-Monocytes,
pubmed-meshheading:17390309-Receptors, G-Protein-Coupled,
pubmed-meshheading:17390309-Tumor Necrosis Factor-alpha
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pubmed:year |
2007
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pubmed:articleTitle |
G protein-coupled receptor 84, a microglia-associated protein expressed in neuroinflammatory conditions.
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pubmed:affiliation |
Department of Oncology and Molecular Endocrinology, Laval University Hospital Research Center, Québec City, Québec, Canada G1V 4G2.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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