| pubmed-article:18485626 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18485626 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:18485626 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:18485626 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
| pubmed-article:18485626 | lifeskim:mentions | umls-concept:C0029463 | lld:lifeskim |
| pubmed-article:18485626 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:18485626 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:18485626 | pubmed:dateCreated | 2008-5-26 | lld:pubmed |
| pubmed-article:18485626 | pubmed:abstractText | The effect of N-(4-hydroxyphenyl) arachidonoyl-ethanolamide (AM404), a drug commonly used to inhibit the anandamide transporter, on intracellular free Ca2+ levels ([Ca2+]i) and viability was studied in human MG63 osteosarcoma cells using the fluorescent dyes fura-2 and WST-1, respectively. AM404 at concentrations > or = 5 microM increased [Ca2+]i in a concentration-dependent manner with an EC50 value of 60 microM. The Ca2+ signal was reduced partly by removing extracellular Ca2+. AM404 induced Mn2+ quench of fura-2 fluorescence implicating Ca2+ influx. The Ca2+ influx was sensitive to La3+, Ni2+, nifedipine and verapamil. In Ca2+-free medium, after pretreatment with 1 microM thapsigargin (an endoplasmic reticulum Ca2+ pump inhibitor), AM404-induced [Ca2+]i rise was abolished; and conversely, AM404 pretreatment totally inhibited thapsigargin-induced [Ca2+]i rise. Inhibition of phospholipase C with U73122 did not change AM404-induced [Ca2+]i rise. At concentrations between 10 and 200 microM, AM404 killed cells in a concentration-dependent manner presumably by inducing apoptotic cell death. The cytotoxic effect of 50 microM AM404 was partly reversed by prechelating cytosolic Ca2+ with BAPTA/AM. Collectively, in MG63 cells, AM404 induced [Ca2+]i rise by causing Ca2+ release from the endoplasmic reticulum in a phospholipase C-independent manner, and Ca2+ influx via L-type Ca2+ channels. AM404 caused cytotoxicity which was possibly mediated by apoptosis. | lld:pubmed |
| pubmed-article:18485626 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18485626 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18485626 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18485626 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:18485626 | pubmed:issn | 0378-4274 | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:ChangHong-Tai... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:WangJue-LongJ... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:JanChung-RenC... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:HuangJong-Khi... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:LuYih-ChauYC | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:TsaiJeng-YuJY | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:ChengHe-Hsiun... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:LinKo-LongKL | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:LiaoWei-Chuan... | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:HsuPei-TePT | lld:pubmed |
| pubmed-article:18485626 | pubmed:author | pubmed-author:HuangChorng-C... | lld:pubmed |
| pubmed-article:18485626 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:18485626 | pubmed:day | 10 | lld:pubmed |
| pubmed-article:18485626 | pubmed:volume | 179 | lld:pubmed |
| pubmed-article:18485626 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18485626 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18485626 | pubmed:pagination | 53-8 | lld:pubmed |
| pubmed-article:18485626 | pubmed:dateRevised | 2008-9-14 | lld:pubmed |
| pubmed-article:18485626 | pubmed:meshHeading | pubmed-meshheading:18485626... | lld:pubmed |
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| pubmed-article:18485626 | pubmed:meshHeading | pubmed-meshheading:18485626... | lld:pubmed |
| pubmed-article:18485626 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18485626 | pubmed:articleTitle | Mechanisms of AM404-induced [Ca(2+)](i) rise and death in human osteosarcoma cells. | lld:pubmed |
| pubmed-article:18485626 | pubmed:affiliation | Department of Surgery, Kaohsiung Veterans General Hospital, Kaohsiung, Taiwan. | lld:pubmed |
| pubmed-article:18485626 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18485626 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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