| pubmed-article:10027760 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C0598829 | lld:lifeskim |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C2700592 | lld:lifeskim |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C1265875 | lld:lifeskim |
| pubmed-article:10027760 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:10027760 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:10027760 | pubmed:dateCreated | 1999-3-2 | lld:pubmed |
| pubmed-article:10027760 | pubmed:abstractText | We studied the effect of thapsigargin on intracellular calcium levels ([Ca2+]i) measured by fura-2 fluorimetry in Madin Darby canine kidney (MDCK) cells. Thapsigargin elevated [Ca2+]i dose dependently with an EC50 of approximately 0.15 microM. The Ca2+ signal consisted of a slow rise, a gradual decay and a plateau. Depletion of the endoplasmic reticulum Ca2+ store with thapsigargin for 7 min abolished the [Ca2+]i increases evoked by bradykinin. Removal of extracellular Ca2+ reduced the thapsigargin response by approximately 50%. The Ca2+ signal was initiated by Ca2+ release from the internal store followed by capacitative Ca2+ entry (CCE). The thapsigargin-evoked CCE was abolished by La3 and Gd3+, and was partly inhibited by SKF 96365 and econazole. After depletion of the internal Ca2+ store for 30 min with another inhibitor of the internal Ca2+ pump, cyclopiazonic acid, thapsigargin failed to increase [Ca2+]i, thus suggesting that the thapsigargin-evoked Ca2+ influx was solely due to CCE. We investigated the mechanism of decay of the thapsigargin response. Pretreatment with La3+ (or Gd3+) or alkalization of extracellular medium to pH 8 significantly potentiated the Ca2+ signal; whereas pretreatment with carbonylcyanide m-chlorophynylhydrozone (CCCP) or removal of extracellular Na+ had no effect. Collectively, our results imply that thapsigargin increased [Ca2+]i in MDCK cells by depleting the internal Ca2+ store followed by CCE, with both pathways contributing equally. The decay of the thapsigargin response might be significantly governed by efflux via the plasmalemmal Ca2+ pump. | lld:pubmed |
| pubmed-article:10027760 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10027760 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10027760 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10027760 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10027760 | pubmed:issn | 0024-3205 | lld:pubmed |
| pubmed-article:10027760 | pubmed:author | pubmed-author:OGOHH | lld:pubmed |
| pubmed-article:10027760 | pubmed:author | pubmed-author:HoC MCM | lld:pubmed |
| pubmed-article:10027760 | pubmed:author | pubmed-author:TsengC JCJ | lld:pubmed |
| pubmed-article:10027760 | pubmed:author | pubmed-author:JanC RCR | lld:pubmed |
| pubmed-article:10027760 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10027760 | pubmed:volume | 64 | lld:pubmed |
| pubmed-article:10027760 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10027760 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10027760 | pubmed:pagination | 259-67 | lld:pubmed |
| pubmed-article:10027760 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:10027760 | pubmed:meshHeading | pubmed-meshheading:10027760... | lld:pubmed |
| pubmed-article:10027760 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10027760 | pubmed:articleTitle | Mechanism of rise and decay of thapsigargin-evoked calcium signals in MDCK cells. | lld:pubmed |
| pubmed-article:10027760 | pubmed:affiliation | Department of Medical Education and Research, Veterans General Hospital-Kaohsiung, National Sun Yat-Sen University, Taiwan, ROC. crjan@isca.vghks.gov.tw | lld:pubmed |
| pubmed-article:10027760 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10027760 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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