pubmed-article:1505923 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1505923 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
pubmed-article:1505923 | lifeskim:mentions | umls-concept:C1882726 | lld:lifeskim |
pubmed-article:1505923 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
pubmed-article:1505923 | lifeskim:mentions | umls-concept:C0540301 | lld:lifeskim |
pubmed-article:1505923 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:1505923 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:1505923 | pubmed:dateCreated | 1992-9-24 | lld:pubmed |
pubmed-article:1505923 | pubmed:abstractText | During liver fibrogenesis, fat-storing cells transform into myofibroblast-like cells and produce increasing amounts of extracellular matrix proteins. Because fat-storing cells produce alpha 2-macroglobulin, an important serine protease inhibitor (serpin), we investigated whether fat-storing cells also synthesize C1-esterase inhibitor, another important serpin. C1-esterase inhibitor synthesis was studied in rat fat-storing cells at day 0, 3 and 7 after isolation by biosynthetic labeling, immunoprecipitation and sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Messenger RNA was examined by Northern-blot analysis. C1-esterase inhibitor gene expression and synthesis were detectable in freshly isolated fat-storing cells and increased distinctly during the time in culture. The cellular source of C1-esterase inhibitor in fat-storing cell cultures was also identified by in situ hybridization of cells at different times after isolation. By inhibition of the N-glycosylation using tunicamycin, rat C1-esterase inhibitor was identified as a glycoprotein. The time course of C1-esterase inhibitor secretion was determined by pulse-chase experiments. C1-esterase inhibitor synthesis was increased 6-fold to 10-fold by interferon-gamma. Specific messenger RNA levels were also raised distinctly by this cytokine. In contrast, interferon-alpha and dexamethasone did not alter C1-esterase inhibitor gene expression. Because C1-esterase inhibitor synthesis is increased by advancing culture time and by the inflammatory mediator interferon-gamma, we suggest that fat-storing cells may enhance the deposition of extracellular matrix proteins by inhibiting their degradation. | lld:pubmed |
pubmed-article:1505923 | pubmed:language | eng | lld:pubmed |
pubmed-article:1505923 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1505923 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1505923 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1505923 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1505923 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1505923 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1505923 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1505923 | pubmed:month | Sep | lld:pubmed |
pubmed-article:1505923 | pubmed:issn | 0270-9139 | lld:pubmed |
pubmed-article:1505923 | pubmed:author | pubmed-author:Meyer zum... | lld:pubmed |
pubmed-article:1505923 | pubmed:author | pubmed-author:RamadoriGG | lld:pubmed |
pubmed-article:1505923 | pubmed:author | pubmed-author:OdenthalMM | lld:pubmed |
pubmed-article:1505923 | pubmed:author | pubmed-author:KnittelTT | lld:pubmed |
pubmed-article:1505923 | pubmed:author | pubmed-author:SchwöglerSS | lld:pubmed |
pubmed-article:1505923 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1505923 | pubmed:volume | 16 | lld:pubmed |
pubmed-article:1505923 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1505923 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1505923 | pubmed:pagination | 794-802 | lld:pubmed |
pubmed-article:1505923 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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pubmed-article:1505923 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1505923 | pubmed:articleTitle | Fat-storing cells of the rat liver synthesize and secrete C1-esterase inhibitor; modulation by cytokines. | lld:pubmed |
pubmed-article:1505923 | pubmed:affiliation | Department of Internal Medicine, University of Mainz, Germany. | lld:pubmed |
pubmed-article:1505923 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1505923 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |