pubmed-article:10764409 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0025914 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0007770 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0056695 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0917729 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C1948027 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
pubmed-article:10764409 | lifeskim:mentions | umls-concept:C0205266 | lld:lifeskim |
pubmed-article:10764409 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:10764409 | pubmed:dateCreated | 2000-5-12 | lld:pubmed |
pubmed-article:10764409 | pubmed:abstractText | Pathological changes of the vasculature are characterized by changes in Ca(2+) handling and alterations in gene expression. In neurons and other cell types, [Ca(2+)](i) often drives changes in gene expression. However, the relationship between Ca(2+) signaling and gene expression in vascular smooth muscle is not well understood. This study examines the ability of Ca(2+) influx through voltage-dependent, L-type Ca(2+) channels (VDCCs) and Ca(2+) release through ryanodine receptors (RyRs) to activate the transcription factor, cAMP-responsive element binding protein (CREB), and increase c-fos levels in intact cerebral arteries. Membrane depolarization increased the fraction of nuclei staining for phosphorylated CREB (P-CREB) and levels of c-fos mRNA in intact mouse cerebral arteries. Ryanodine, which inhibits RyRs, increased P-CREB staining and c-fos levels. Forskolin, an activator of adenylyl cyclase, and sodium nitroprusside, an NO donor, increased P-CREB and c-fos levels. Nisoldipine, an inhibitor of VDCCs, reversed the effects of depolarization and ryanodine on P-CREB and c-fos levels, but not the effects of forskolin or sodium nitroprusside. Inhibition of Ca(2+)/calmodulin-dependent protein kinase (CaM kinase) blocked increases in P-CREB and c-fos levels seen with membrane depolarization, suggesting that CaM kinase has an important role in the pathway leading from Ca(2+) influx to CREB-mediated changes in c-fos levels. Our data suggest that membrane depolarization increases [Ca(2+)](i) through activation of VDCCs, leading to increased P-CREB and c-fos, and that RyRs have a profound effect on this pathway by indirectly regulating Ca(2+) entry through VDCCs. These results provide the first evidence of Ca(2+) regulation of CREB and c-fos in arterial smooth muscle. | lld:pubmed |
pubmed-article:10764409 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:language | eng | lld:pubmed |
pubmed-article:10764409 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:10764409 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:10764409 | pubmed:month | Apr | lld:pubmed |
pubmed-article:10764409 | pubmed:issn | 1524-4571 | lld:pubmed |
pubmed-article:10764409 | pubmed:author | pubmed-author:NelsonM TMT | lld:pubmed |
pubmed-article:10764409 | pubmed:author | pubmed-author:LounsburyK... | lld:pubmed |
pubmed-article:10764409 | pubmed:author | pubmed-author:CartinLL | lld:pubmed |
pubmed-article:10764409 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:10764409 | pubmed:day | 14 | lld:pubmed |
pubmed-article:10764409 | pubmed:volume | 86 | lld:pubmed |
pubmed-article:10764409 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:10764409 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:10764409 | pubmed:pagination | 760-7 | lld:pubmed |
pubmed-article:10764409 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:10764409 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:10764409 | pubmed:articleTitle | Coupling of Ca(2+) to CREB activation and gene expression in intact cerebral arteries from mouse : roles of ryanodine receptors and voltage-dependent Ca(2+) channels. | lld:pubmed |
pubmed-article:10764409 | pubmed:affiliation | Department of Pharmacology, University of Vermont, Burlington, VT, USA. | lld:pubmed |
pubmed-article:10764409 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:10764409 | pubmed:publicationType | In Vitro | lld:pubmed |
pubmed-article:10764409 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:10764409 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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