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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0019564,
umls-concept:C0035696,
umls-concept:C0077204,
umls-concept:C0175677,
umls-concept:C0205263,
umls-concept:C0442043,
umls-concept:C0600251,
umls-concept:C0702240,
umls-concept:C0871261,
umls-concept:C1456820,
umls-concept:C1515406,
umls-concept:C1660642,
umls-concept:C1704256,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2911692
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pubmed:issue |
4
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pubmed:dateCreated |
1998-10-14
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pubmed:abstractText |
In certain pathologic states, cytokine production may become spatially and temporally dysregulated, leading to their inappropriate production and potentially detrimental consequences. Tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, IL-6, and transforming growth factor-beta (TGF-beta) mediate a range of host responses affecting multiple cell types. To study the role of cytokines in the early stages of brain injury, we examined alterations in the 17-day-old mouse hippocampus during trimethyltin-induced neurodegeneration characterized by neuronal necrosis, microglia activation in the dentate, and astrocyte reactivity throughout the hippocampus. By 24 h after dosing, elevations in mRNA levels for TNF-alpha, IL-1alpha, IL-1beta, and IL-6 mRNA were seen. TGF-beta1 mRNA was elevated at 72 h. In situ hybridization showed that TNF-alpha and IL-1alpha were localized to the microglia, whereas TGF-beta1 was expressed predominantly in hippocampal pyramidal cells. Intercellular adhesion molecule-1, EB-22, Mac-1, and glial fibrillary acidic protein mRNA levels were elevated within the first 3 days of exposure in the absence of increased inducible nitric oxide synthetase and interferon-gamma mRNA. These data suggest that pro-inflammatory cytokines contribute to the progression and pattern of neuronal degeneration in the hippocampus.
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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/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Ribonucleases,
http://linkedlifedata.com/resource/pubmed/chemical/Synaptophysin,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/Trimethyltin Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/trimethyltin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0022-3042
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
71
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1577-87
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:9751191-Animals,
pubmed-meshheading:9751191-Hippocampus,
pubmed-meshheading:9751191-Immunohistochemistry,
pubmed-meshheading:9751191-In Situ Hybridization,
pubmed-meshheading:9751191-Interleukin-1,
pubmed-meshheading:9751191-Male,
pubmed-meshheading:9751191-Mice,
pubmed-meshheading:9751191-RNA, Messenger,
pubmed-meshheading:9751191-Ribonucleases,
pubmed-meshheading:9751191-Synaptophysin,
pubmed-meshheading:9751191-Time Factors,
pubmed-meshheading:9751191-Transforming Growth Factor beta,
pubmed-meshheading:9751191-Trimethyltin Compounds,
pubmed-meshheading:9751191-Tumor Necrosis Factor-alpha
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pubmed:year |
1998
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pubmed:articleTitle |
Cellular localization and temporal elevation of tumor necrosis factor-alpha, interleukin-1 alpha, and transforming growth factor-beta 1 mRNA in hippocampal injury response induced by trimethyltin.
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pubmed:affiliation |
Laboratory of Neurotoxicology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, North Carolina 17709, USA.
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pubmed:publicationType |
Journal Article
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