| pubmed-article:18836030 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C1267092 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0225336 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0034052 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C1383501 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0442805 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:18836030 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18836030 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:18836030 | pubmed:dateCreated | 2008-12-2 | lld:pubmed |
| pubmed-article:18836030 | pubmed:abstractText | Thrombin is a procoagulant inflammatory agonist that can disrupt the endothelium-lumen barrier in the lung by causing contraction of endothelial cells and promote pulmonary cell proliferation. Both contraction and proliferation require increases in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)). In this study, we compared the effect of thrombin on Ca(2+) signaling in human pulmonary artery smooth muscle (PASMC) and endothelial (PAEC) cells. Thrombin increased the [Ca(2+)](cyt) in both cell types; however, the transient response was significantly higher and recovered quicker in the PASMC, suggesting different mechanisms may contribute to thrombin-mediated increases in [Ca(2+)](cyt) in these cell types. Depletion of intracellular stores with cyclopiazonic acid (CPA) in the absence of extracellular Ca(2+) induced calcium transients representative of those observed in response to thrombin in both cell types. Interestingly, CPA pretreatment significantly attenuated thrombin-induced Ca(2+) release in PASMC; this attenuation was not apparent in PAEC, indicating that a PAEC-specific mechanism was targeted by thrombin. Treatment with a combination of CPA, caffeine, and ryanodine also failed to abolish the thrombin-induced Ca(2+) transient in PAEC. Notably, thrombin-induced receptor-mediated calcium influx was still observed in PASMC after CPA pretreatment in the presence of extracellular Ca(2+). Ca(2+) oscillations were triggered by thrombin in PASMC resulting from a balance of extracellular Ca(2+) influx and Ca(2+) reuptake by the sarcoplasmic reticulum. The data show that thrombin induces increases in intracellular calcium in PASMC and PAEC with a distinct CPA-, caffeine-, and ryanodine-insensitive release existing only in PAEC. Furthermore, a dynamic balance between Ca(2+) influx, intracellular Ca(2+) release, and reuptake underlie the Ca(2+) transients evoked by thrombin in some PASMC. Understanding of such mechanisms will provide an important insight into thrombin-mediated vascular injury during hypertension. | lld:pubmed |
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| pubmed-article:18836030 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18836030 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18836030 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18836030 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18836030 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:18836030 | pubmed:issn | 1040-0605 | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:YuanJason... | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:RemillardCarm... | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:KoEun AEA | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:SacksRichard... | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:AgangeNeginN | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:FirthAmy LAL | lld:pubmed |
| pubmed-article:18836030 | pubmed:author | pubmed-author:YauJocelynJ | lld:pubmed |
| pubmed-article:18836030 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18836030 | pubmed:volume | 295 | lld:pubmed |
| pubmed-article:18836030 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18836030 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18836030 | pubmed:pagination | L1048-55 | lld:pubmed |
| pubmed-article:18836030 | pubmed:dateRevised | 2010-9-21 | lld:pubmed |
| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
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| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
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| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
| pubmed-article:18836030 | pubmed:meshHeading | pubmed-meshheading:18836030... | lld:pubmed |
| pubmed-article:18836030 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18836030 | pubmed:articleTitle | Thrombin-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells. | lld:pubmed |
| pubmed-article:18836030 | pubmed:affiliation | Division of Pulmonary and Critical Care Medicine, Dept. of Medicine, Univ. of California, San Diego, 9500 Gilman Drive, MC 0725, La Jolla, CA 92093-0725,USA. | lld:pubmed |
| pubmed-article:18836030 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18836030 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
| entrez-gene:2151 | entrezgene:pubmed | pubmed-article:18836030 | lld:entrezgene |
| http://linkedlifedata.com/r... | entrezgene:pubmed | pubmed-article:18836030 | lld:entrezgene |
