| pubmed-article:11102468 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11102468 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:11102468 | lifeskim:mentions | umls-concept:C0021760 | lld:lifeskim |
| pubmed-article:11102468 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:11102468 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:11102468 | pubmed:dateCreated | 2001-1-4 | lld:pubmed |
| pubmed-article:11102468 | pubmed:abstractText | Interleukin-6 (IL-6) has neuromodulatory and neuroprotective effects in vivo. It is expressed in glial cells and neurons both under physiological conditions and in various neurological diseases. Although the expression of IL-6 in glia has been intensely investigated, little is known about the regulation of IL-6 production by neurons. Therefore, we investigated the regulation of IL-6 expression in neurons. Membrane depolarization raised IL-6 mRNA accumulation in primary cortical cells and the PC-12 cell line. In vivo, IL-6 mRNA in the brain increased significantly after epileptic seizures. To investigate IL-6 gene transcription, PC-12 cells were transfected with reporter gene constructs containing the human IL-6 promoter. Membrane depolarization raised IL-6 transcription twofold to fourfold. This increase could be blocked by lowering extracellular Ca(2+) levels or by inhibiting L-type Ca(2+) channels or Ca(2+)/calmodulin-dependent protein kinases. Internal mutations in various elements of the IL-6 promoter revealed the glucocorticoid response element (GRE) 2 to be a depolarization-responsive element. Although the GRE2 bound the glucocorticoid receptor (GR) and was stimulated by dexamethasone, the GR was not responsible for the effect of membrane depolarization because a consensus GRE did not mediate stimulation by membrane depolarization. Instead, another yet undefined factor that binds to the IL-6 GRE2 may mediate the response to membrane depolarization. These data demonstrate that the expression of IL-6 in neurons is regulated by membrane depolarization and suggest a novel Ca(2+)-responsive promoter element. Through this mechanism, IL-6 may function as a neuromodulator induced by neuronal activity. | lld:pubmed |
| pubmed-article:11102468 | pubmed:language | eng | lld:pubmed |
| pubmed-article:11102468 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:11102468 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11102468 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:11102468 | pubmed:issn | 1529-2401 | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:PetersenNN | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:SchwaningerMM | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:WeiserTT | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:PrinsLL | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:JüttlerEE | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:KnopfUU | lld:pubmed |
| pubmed-article:11102468 | pubmed:author | pubmed-author:SallmannSS | lld:pubmed |
| pubmed-article:11102468 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:11102468 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:11102468 | pubmed:volume | 20 | lld:pubmed |
| pubmed-article:11102468 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11102468 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11102468 | pubmed:pagination | 8637-42 | lld:pubmed |
| pubmed-article:11102468 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11102468 | pubmed:year | 2000 | lld:pubmed |
| pubmed-article:11102468 | pubmed:articleTitle | Induction of interleukin-6 by depolarization of neurons. | lld:pubmed |
| pubmed-article:11102468 | pubmed:affiliation | Department of Neurology, University of Heidelberg, 69120 Heidelberg, Germany. | lld:pubmed |
| pubmed-article:11102468 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:11102468 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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