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| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0022567 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0043240 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0221912 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0079189 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C1533698 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0700114 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0333348 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
| pubmed-article:9856818 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
| pubmed-article:9856818 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:9856818 | pubmed:dateCreated | 1999-1-4 | lld:pubmed |
| pubmed-article:9856818 | pubmed:abstractText | Recently we demonstrated a strong expression of inducible nitric oxide synthase (iNOS) and GTP-cyclohydrolase I (GTP-CH I) in the basal keratinocytes of the epidermis adjacent to the wound and of the hyperproliferative epithelium during wound healing. To identify possible mediators of iNOS and GTP-CH I expression during this process, we analyzed the regulation of iNOS and GTP-CH I expression in cultured human keratinocytes. We found a large and long lasting coinduction of iNOS and GTP-CH I expression upon simultaneous treatment of quiescent cells with inflammatory cytokines interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma, but not with serum growth factors. The stimulatory effect of interleukin-1beta, tumor necrosis factor-alpha, and interferon-gamma is strongly synergistic on iNOS and GTP-CH I expression, because these factors alone stimulated GTP-CH I expression, although to a much lesser extent. Furthermore, iNOS mRNA levels are not influenced at all by stimulation with IL-1beta and revealed only a weak induction after treatment with tumor necrosis factor-alpha and interferon-gamma. Induction of iNOS and GTP-CH I gene expression upon cytokine and interferon-gamma exposure is independent of de novo protein synthesis. Because these cytokines are present at the wound site, they might be responsible for iNOS and GTP-CH I induction during cutaneous repair. Serum, which is released upon hemorrhage, is likely to play no stimulatory role in iNOS and GTP-CH I induction during wound healing. | lld:pubmed |
| pubmed-article:9856818 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9856818 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9856818 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:9856818 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9856818 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:9856818 | pubmed:issn | 0022-202X | lld:pubmed |
| pubmed-article:9856818 | pubmed:author | pubmed-author:FrankSS | lld:pubmed |
| pubmed-article:9856818 | pubmed:author | pubmed-author:WernerE RER | lld:pubmed |
| pubmed-article:9856818 | pubmed:author | pubmed-author:KolfJJ | lld:pubmed |
| pubmed-article:9856818 | pubmed:author | pubmed-author:Pfeilschifter... | lld:pubmed |
| pubmed-article:9856818 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9856818 | pubmed:volume | 111 | lld:pubmed |
| pubmed-article:9856818 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9856818 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9856818 | pubmed:pagination | 1065-71 | lld:pubmed |
| pubmed-article:9856818 | pubmed:dateRevised | 2011-10-27 | lld:pubmed |
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| pubmed-article:9856818 | pubmed:year | 1998 | lld:pubmed |
| pubmed-article:9856818 | pubmed:articleTitle | Coordinated induction of inducible nitric oxide synthase and GTP-cyclohydrolase I is dependent on inflammatory cytokines and interferon-gamma in HaCaT keratinocytes: implications for the model of cutaneous wound repair. | lld:pubmed |
| pubmed-article:9856818 | pubmed:affiliation | Zentrum der Pharmakologie, Klinikum der Johann Wolfgang Goethe-Universität, Frankfurt am Main, Germany. | lld:pubmed |
| pubmed-article:9856818 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9856818 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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