Source:http://linkedlifedata.com/resource/pubmed/id/20949361
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2010-11-10
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pubmed:abstractText |
Non-thyroidal illness is characterized by low tri-iodothyronine (T3) serum level under acute-phase conditions. We studied hepatic gene expression of the newly identified thyroid hormone receptor (TR) cofactor DOR/TP53INP2 together with TRs in a rat model of aseptic abscesses induced by injecting intramuscular turpentine-oil into each hind limb. A fast (4-6 h) decrease in the serum level of free thyroxine and free T3 was observed. By immunohistology, abundant DOR protein expression was detected in the nuclei of hepatocytes and ED-1(+) (mononuclear phagocytes), CK-19(+) (biliary cells), and SMA(+) (mesenchymal cells of the portal tract) cells. DOR signal was reduced with a minimum at 6-12 h after the acute-phase reaction (APR). Immunohistology also showed a similar pattern of protein expression in TR?1 but without a significant change during APR. Transcripts specific for DOR, nuclear receptor co-repressor 1 (NCoR-1), and TR?1 were down-regulated with a minimum at 6-12 h, whereas expression for TR?1 and TR?2 was slightly and significantly up-regulated, respectively, with a maximum at 24 h after APR was initiated. In cultured hepatocytes, acute-phase cytokines interleukin-1? (IL-1?) and IL-6 down-regulated DOR and TR?1 at the mRNA level. Moreover, gene expression of DOR and TRs (TR?1, TR?2, and TR?1) was up-regulated in hepatocytes by adding T3 to the culture medium; this up-regulation was almost completely blocked by treating the cells with IL-6. Thus, TR?1, NCoR-1, and the recently identified DOR/TP53INP2 are abundantly expressed and down-regulated in liver cells during APR. Their down-regulation is attributable to the decreased serum level of thyroid hormones and most probably also to the direct action of the main acute-phase cytokines.
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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/DOR protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/Muscle Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Ncor1 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Receptor Co-Repressor 1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thyroid Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Thyroxine,
http://linkedlifedata.com/resource/pubmed/chemical/Triiodothyronine,
http://linkedlifedata.com/resource/pubmed/chemical/Turpentine
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1432-0878
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
342
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
261-72
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pubmed:meshHeading |
pubmed-meshheading:20949361-Acute-Phase Reaction,
pubmed-meshheading:20949361-Animals,
pubmed-meshheading:20949361-Cells, Cultured,
pubmed-meshheading:20949361-Disease Models, Animal,
pubmed-meshheading:20949361-Drug Therapy, Combination,
pubmed-meshheading:20949361-Gene Expression,
pubmed-meshheading:20949361-Hepatocytes,
pubmed-meshheading:20949361-Interleukin-6,
pubmed-meshheading:20949361-Liver,
pubmed-meshheading:20949361-Male,
pubmed-meshheading:20949361-Muscle Proteins,
pubmed-meshheading:20949361-Nuclear Receptor Co-Repressor 1,
pubmed-meshheading:20949361-RNA, Messenger,
pubmed-meshheading:20949361-Rats,
pubmed-meshheading:20949361-Rats, Wistar,
pubmed-meshheading:20949361-Receptors, Thyroid Hormone,
pubmed-meshheading:20949361-Thyroxine,
pubmed-meshheading:20949361-Triiodothyronine,
pubmed-meshheading:20949361-Turpentine,
pubmed-meshheading:20949361-Up-Regulation
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pubmed:year |
2010
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pubmed:articleTitle |
Changes in gene expression of DOR and other thyroid hormone receptors in rat liver during acute-phase response.
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pubmed:affiliation |
Division of Gastroenterology and Endocrinology, Department of Internal Medicine, University Medical Center, Georg August University, Göttingen, Germany. i.malik@med.uni-goettingen.de
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pubmed:publicationType |
Journal Article
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