Source:http://linkedlifedata.com/resource/pubmed/id/16473887
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
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| pubmed:dateCreated |
2006-4-3
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| pubmed:abstractText |
Many neurological insults are accompanied by a marked acute inflammatory reaction, involving the activation of microglia. Using a model of exogenous application of fluorescence-labeled BV2 microglia in pathophysiologically relevant concentrations onto organotypic hippocampal slice cultures, we investigated the specific effects of microglia on neuronal damage after ischemic injury. Neuronal cell death after oxygen-glucose deprivation (OGD) was determined by propidium iodide incorporation and Nissl staining. Migration and interaction with neurons were analyzed by time resolved 3-D two-photon microscopy. We show that microglia protect against OGD-induced neuronal damage and engage in close physical cell-cell contact with neurons in the damaged brain area. Neuroprotection and migration of microglia were not seen with integrin regulator CD11a-deficient microglia or HL-60 granulocytes. The induction of migration and neuron-microglia interaction deep inside the slice was markedly increased under OGD conditions. Lipopolysaccharide-prestimulated microglia failed to provide neuroprotection after OGD. Pharmacological interference with microglia function resulted in a reduced neuroprotection. Microglia proved to be neuroprotective even when applied up to 4 h after OGD, thus defining a "protective time window." In acute injury such as trauma or stroke, appropriately activated microglia may primarily have a neuroprotective role. Anti-inflammatory treatment within the protective time window of microglia would therefore be counterintuitive.
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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/Anisomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Bacterial Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD11a,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Minocycline
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| pubmed:status |
MEDLINE
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| pubmed:month |
Apr
|
| pubmed:issn |
1530-6860
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
20
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
714-6
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:16473887-Animals,
pubmed-meshheading:16473887-Anisomycin,
pubmed-meshheading:16473887-Anoxia,
pubmed-meshheading:16473887-Anti-Bacterial Agents,
pubmed-meshheading:16473887-Antigens, CD11a,
pubmed-meshheading:16473887-Brain Ischemia,
pubmed-meshheading:16473887-Cell Death,
pubmed-meshheading:16473887-Cell Line,
pubmed-meshheading:16473887-Glucose,
pubmed-meshheading:16473887-Granulocytes,
pubmed-meshheading:16473887-HL-60 Cells,
pubmed-meshheading:16473887-Hippocampus,
pubmed-meshheading:16473887-Humans,
pubmed-meshheading:16473887-Mice,
pubmed-meshheading:16473887-Mice, Transgenic,
pubmed-meshheading:16473887-Microglia,
pubmed-meshheading:16473887-Minocycline,
pubmed-meshheading:16473887-Neurons,
pubmed-meshheading:16473887-Rats,
pubmed-meshheading:16473887-Rats, Wistar
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| pubmed:year |
2006
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| pubmed:articleTitle |
Microglia provide neuroprotection after ischemia.
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| pubmed:affiliation |
Leibniz Institute for Neurobiology, Project Group Neuropharmacology, Magdeburg, Germany.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|