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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2-3
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pubmed:dateCreated |
2005-12-26
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pubmed:abstractText |
Elucidating the relationship of glutamate-induced Ca2+ flux and oxidative death of neuronal cells may be of great relevance for neurodegenerative diseases in human beings. Mouse hippocampal HT22 cells provide a model system to study this relationship at the molecular level. Here we show that stimulation of HT22 cells with 5 mM glutamate is cytotoxic. Glutamate-induced cytotoxicity was associated with the generation of reactive oxygen species (ROS) and activation of the death executioner caspases 1 and 3. Treatment of HT22 cells with the calcium chelator, EGTA, and the calcium channel blocker, CoCl2, revealed that glutamate-induced cell death was dependent, in part, on glutamate-induced Ca2+ influx from extracellular stores. However, activation of caspases 1 and 3 and death of HT22 cells were also observed when Ca2+ was lacking in the extracellular milieu and ROS production abrogated. These findings led us to conclude that glutamate-induced death of mouse HT22 cells utilizes a complex mechanism that relies only in part on Ca2+ influx and ROS production. Additional studies are warranted to evaluate glutamate-induced death mechanisms that operate independently of Ca2+ influx and generation of ROS.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CASP3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Casp3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Chelating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Cobalt,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/acetyl-aspartyl-glutamyl-valyl-aspar...,
http://linkedlifedata.com/resource/pubmed/chemical/cobaltous chloride
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0304-3940
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
393
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
165-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:16229947-Animals,
pubmed-meshheading:16229947-Calcium,
pubmed-meshheading:16229947-Calcium Chloride,
pubmed-meshheading:16229947-Caspase 3,
pubmed-meshheading:16229947-Caspases,
pubmed-meshheading:16229947-Cell Count,
pubmed-meshheading:16229947-Cell Death,
pubmed-meshheading:16229947-Cell Line,
pubmed-meshheading:16229947-Cell Survival,
pubmed-meshheading:16229947-Chelating Agents,
pubmed-meshheading:16229947-Cobalt,
pubmed-meshheading:16229947-Dose-Response Relationship, Drug,
pubmed-meshheading:16229947-Drug Interactions,
pubmed-meshheading:16229947-Egtazic Acid,
pubmed-meshheading:16229947-Extracellular Space,
pubmed-meshheading:16229947-Glutamic Acid,
pubmed-meshheading:16229947-Mice,
pubmed-meshheading:16229947-Neurons,
pubmed-meshheading:16229947-Oligopeptides,
pubmed-meshheading:16229947-Oxidative Stress,
pubmed-meshheading:16229947-Reactive Oxygen Species
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pubmed:year |
2006
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pubmed:articleTitle |
Glutamate-induced oxidative stress, but not cell death, is largely dependent upon extracellular calcium in mouse neuronal HT22 cells.
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pubmed:affiliation |
Systemic Proteomics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 52 Oun, Yusong, Taejon 305-333, South Korea.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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