Source:http://linkedlifedata.com/resource/pubmed/id/10700554
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1-2
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| pubmed:dateCreated |
2000-5-4
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| pubmed:abstractText |
Glutamate-induced excitotoxicity, with certain characteristics of apoptosis, has been implicated in a variety of neuronal degenerative disorders. In some physiological cases, extracellular signal-regulated kinases (ERK1/2) are activated by stimulation of glutamate receptors. In the present study, the activation (diphosphorylation) and role of ERK1/2 in glutamate-induced apoptotic-like death in cultured cortical neurons were investigated. Protein levels and activation (diphosphorylation) levels of ERK1/2 were examined by Western immunoblot, probed with anti-ERK1/2 and anti-active (diphosphorylated) ERK1/2 antibodies, respectively. Apoptotic-like death was determined by DAPI staining. Before a remarkable increase of apoptotic-like cell death was observed at 9-18 h after 15 min exposure to 50 microM glutamate, diphosphorylation levels of ERK1/2 were rapidly increased, peaked at 5-15 min of the exposure, and reverted to sham control level 3 h after the exposure, while the protein levels of ERK1/2 were unaffected. The glutamate concentration effective for inducing apoptotic-like cell death was correlated with that for inducing ERK1/2 diphosphorylation. Both ERK1/2 diphosphorylation and the apoptotic-like cell death were largely prevented by MK-801, a specific NMDA receptor (a subtype receptor of glutamate) antagonist, or the elimination of extracellular Ca(2+) with EGTA. PD98059, a specific inhibitor of ERK1/2 kinase, completely inhibited ERK1/2 diphosphorylation and partially inhibited the apoptotic-like cell death. These results suggest that largely via NMDA receptor-mediated influx of extracellular Ca(2+), ERK1/2 were rapidly and transiently activated and were involved in glutamate-induced apoptotic-like death in cultured rat cortical neurons.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Chelating Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Dizocilpine Maleate,
http://linkedlifedata.com/resource/pubmed/chemical/Egtazic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Excitatory Amino Acid Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Flavonoids,
http://linkedlifedata.com/resource/pubmed/chemical/Glutamic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 1,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Neurotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/PD 98059
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| pubmed:status |
MEDLINE
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| pubmed:month |
Feb
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| pubmed:issn |
0006-8993
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
28
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| pubmed:volume |
857
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
71-7
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:10700554-Animals,
pubmed-meshheading:10700554-Apoptosis,
pubmed-meshheading:10700554-Cell Culture Techniques,
pubmed-meshheading:10700554-Cerebral Cortex,
pubmed-meshheading:10700554-Chelating Agents,
pubmed-meshheading:10700554-Dizocilpine Maleate,
pubmed-meshheading:10700554-Egtazic Acid,
pubmed-meshheading:10700554-Embryo, Mammalian,
pubmed-meshheading:10700554-Enzyme Inhibitors,
pubmed-meshheading:10700554-Excitatory Amino Acid Antagonists,
pubmed-meshheading:10700554-Flavonoids,
pubmed-meshheading:10700554-Glutamic Acid,
pubmed-meshheading:10700554-Mitogen-Activated Protein Kinase 1,
pubmed-meshheading:10700554-Mitogen-Activated Protein Kinase 3,
pubmed-meshheading:10700554-Mitogen-Activated Protein Kinases,
pubmed-meshheading:10700554-Neurons,
pubmed-meshheading:10700554-Neurotoxins,
pubmed-meshheading:10700554-Phosphorylation,
pubmed-meshheading:10700554-Rats,
pubmed-meshheading:10700554-Rats, Sprague-Dawley,
pubmed-meshheading:10700554-Time Factors
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| pubmed:year |
2000
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| pubmed:articleTitle |
Diphosphorylation and involvement of extracellular signal-regulated kinases (ERK1/2) in glutamate-induced apoptotic-like death in cultured rat cortical neurons.
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| pubmed:affiliation |
Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, 84 West Huai-hai Road, Xuzhou, China.
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| pubmed:publicationType |
Journal Article
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