Source:http://linkedlifedata.com/resource/pubmed/id/16107267
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2005-10-31
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pubmed:abstractText |
To determine critical role of cyclooxygenase-2 (COX-2) for development of viral myocarditis, a mouse model of encephalomyocarditis virus-induced myocarditis was used. The virus was intraperitoneally given to COX-2 gene-deficient heterozygote mice (COX-2+/-) and wild-type mice (WT). We examined differences in heart weights, cardiac histological scores, numbers of infiltrating or apoptotic cells in myocardium, cardiac expression levels of COX-2, tumor necrosis factor-alpha (TNF-alpha), and adiponectin mRNA, immunoreactivity of COX-2, TNF-alpha, and adiponectin in myocytes, cardiac concentrations of TNF-alpha and adiponectin, prostaglandin E2 (PGE2) levels in hearts, and viral titers in tissues between COX-2+/- and WT. We observed significantly decreased expression of COX-2 mRNA and reactivity in hearts from COX-2+/- on day 8 after viral inoculation as compared with that from WT, together with elevated cardiac weights and severe inflammatory myocardial damage in COX-2+/-. Cardiac expression of TNF-alpha mRNA, reactivity, and protein on day 8 was significantly higher in COX-2+/- than in WT, together with reciprocal expression of adiponectin mRNA, reactivity, and protein in hearts. Significantly reduced cardiac PGE2 levels on day 8 were found in COX-2+/- compared with those in WT. There was no difference in local viral titers between both groups on day 4. Infected WT treated with a selective COX-2 inhibitor, NS-398, also showed the augmented myocardial damage on day 8. These results suggest that inhibition of COX-2 may enhance myocardial damage through reciprocal cardiac expression of TNF-alpha and adiponectin in a mouse model of viral myocarditis.
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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/Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooxygenase 2 Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone,
http://linkedlifedata.com/resource/pubmed/chemical/N-(2-cyclohexyloxy-4-nitrophenyl)met...,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrobenzenes,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfonamides,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0024-3205
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
26
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pubmed:volume |
78
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
195-204
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16107267-Adiponectin,
pubmed-meshheading:16107267-Animals,
pubmed-meshheading:16107267-Body Weight,
pubmed-meshheading:16107267-Cardiovirus Infections,
pubmed-meshheading:16107267-Cyclooxygenase 2,
pubmed-meshheading:16107267-Cyclooxygenase 2 Inhibitors,
pubmed-meshheading:16107267-Dinoprostone,
pubmed-meshheading:16107267-Encephalomyocarditis virus,
pubmed-meshheading:16107267-Mice,
pubmed-meshheading:16107267-Mice, Inbred C57BL,
pubmed-meshheading:16107267-Mice, Knockout,
pubmed-meshheading:16107267-Myocarditis,
pubmed-meshheading:16107267-Myocardium,
pubmed-meshheading:16107267-Myocytes, Cardiac,
pubmed-meshheading:16107267-Nitrobenzenes,
pubmed-meshheading:16107267-Organ Size,
pubmed-meshheading:16107267-RNA, Messenger,
pubmed-meshheading:16107267-Sulfonamides,
pubmed-meshheading:16107267-Tumor Necrosis Factor-alpha
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pubmed:year |
2005
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pubmed:articleTitle |
Inhibition of cyclooxygenase-2 enhances myocardial damage in a mouse model of viral myocarditis.
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pubmed:affiliation |
Department of a General Medicine, Kanazawa Medical University, Uchinada-machi, Kahoku-gun, Ishikawa 920-0293, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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