| pubmed-article:2788696 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2788696 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:2788696 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:2788696 | lifeskim:mentions | umls-concept:C1420709 | lld:lifeskim |
| pubmed-article:2788696 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:2788696 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:2788696 | pubmed:dateCreated | 1989-10-3 | lld:pubmed |
| pubmed-article:2788696 | pubmed:abstractText | The regulation of thyroglobulin (Tg) and its specific mRNA by interleukin-1 (IL-1) in cultured human thyrocytes was investigated. Specific binding of 125I-labelled IL-1 on thyrocytes was confirmed by solid-phase binding assay. Thyrocytes dispersed from Graves' thyroid tissues were incubated with TSH with or without recombinant human IL-1. TSH stimulated Tg release from cultured human thyrocytes in a dose- and time-dependent manner. Both IL-1 alpha and beta inhibited TSH-induced Tg release at concentrations ranging from 0.01 to 10 U/ml. The suppressive activities of IL-1 alpha and beta were similar. They did not alter the basal level of Tg release. Unstimulated human thyrocytes did not contain any detectable Tg mRNA, but TSH-stimulated thyrocytes expressed a single species of Tg mRNA (8.5 kb). Both IL-1 alpha and beta inhibited TSH-induced Tg mRNA in a dose-responsive manner. IL-1 (10 U/ml) caused maximal suppression of TSH-induced Tg mRNA to nearly basal levels. In contrast, the gamma-actin mRNA hybridization signal was not altered in control or treated cells. Furthermore, IL-1 stimulated [3H]thymidine uptake into thyrocyte DNA. These results demonstrate that IL-1 directly inhibits TSH-induced Tg gene expression and provide further support for a functional role of IL-1 as a local modulator of thyroid hormone synthesis. | lld:pubmed |
| pubmed-article:2788696 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2788696 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2788696 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2788696 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:2788696 | pubmed:issn | 0022-0795 | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:KimuraHH | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:YamashitaSS | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:NagatakiSS | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:NagayamaYY | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:IzumiMM | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:AshizawaKK | lld:pubmed |
| pubmed-article:2788696 | pubmed:author | pubmed-author:HirayuHH | lld:pubmed |
| pubmed-article:2788696 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2788696 | pubmed:volume | 122 | lld:pubmed |
| pubmed-article:2788696 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2788696 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2788696 | pubmed:pagination | 177-83 | lld:pubmed |
| pubmed-article:2788696 | pubmed:dateRevised | 2004-11-17 | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:meshHeading | pubmed-meshheading:2788696-... | lld:pubmed |
| pubmed-article:2788696 | pubmed:year | 1989 | lld:pubmed |
| pubmed-article:2788696 | pubmed:articleTitle | Interleukin-1 inhibits thyrotrophin-induced human thyroglobulin gene expression. | lld:pubmed |
| pubmed-article:2788696 | pubmed:affiliation | First Department of Internal Medicine, Nagasaki University School of Medicine, Japan. | lld:pubmed |
| pubmed-article:2788696 | pubmed:publicationType | Journal Article | lld:pubmed |
