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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0018284,
umls-concept:C0028128,
umls-concept:C0162638,
umls-concept:C0185117,
umls-concept:C0205263,
umls-concept:C0376515,
umls-concept:C0392747,
umls-concept:C0443172,
umls-concept:C0521390,
umls-concept:C2911684
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pubmed:issue |
10
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pubmed:dateCreated |
1999-5-6
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pubmed:abstractText |
Recent studies have shown that nitric oxide (NO) donors can trigger apoptosis of neurons, and growth factors such as insulin-like growth factor-1 (IGF-1) and basic fibroblast growth factor (bFGF) can protect against NO-induced neuronal cell death. The purpose of this study was to elucidate the possible mechanisms of NO-mediated neuronal apoptosis and the neuroprotective action of these growth factors. Both IGF-1 and bFGF prevented apoptosis induced by NO donors, sodium nitroprusside (SNP) or 3-morpholinosydnonimin (SIN-1) in hippocampal neuronal cultures. Incubation of neurons with SNP induced caspase-3-like activation following downregulation of Bcl-2 and upregulation of Bax protein levels in cultured neurons. Treatment of neurons with a bax antisense oligonucleotide inhibited the caspase-3-like activation and neuronal death induced by SNP. In addition, treatment of neurons with an inhibitor of caspase-3, Ac-DEVD-CHO, together with SNP did not affect the changes in the protein levels, although it inhibited NO-induced cell death. Pretreatment of cultures with either IGF-1 or bFGF prior to NO exposure inhibited caspase-3-like activation together with the changes in Bcl-2 and Bax protein levels. These results suggest that the changes in Bcl-2 and Bax protein levels followed by caspase-3-like activation are a component in the cascade of NO-induced neuronal apoptosis, and that the neuroprotective actions of IGF-1 and bFGF might be due to inhibition of the changes in the protein levels of the Bcl-2 family.
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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/3-morpholino-sydnonimine,
http://linkedlifedata.com/resource/pubmed/chemical/Bax protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Casp3 protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspases,
http://linkedlifedata.com/resource/pubmed/chemical/Cysteine Proteinase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Fibroblast Growth Factor 2,
http://linkedlifedata.com/resource/pubmed/chemical/Growth Substances,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin-Like Growth Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/Molsidomine,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide,
http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Donors,
http://linkedlifedata.com/resource/pubmed/chemical/Nitroprusside,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/acetyl-aspartyl-glutamyl-valyl-aspar...,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-2-Associated X Protein
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1350-9047
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
911-9
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:10203697-Animals,
pubmed-meshheading:10203697-Apoptosis,
pubmed-meshheading:10203697-Caspase 3,
pubmed-meshheading:10203697-Caspases,
pubmed-meshheading:10203697-Cell Survival,
pubmed-meshheading:10203697-Cells, Cultured,
pubmed-meshheading:10203697-Cysteine Proteinase Inhibitors,
pubmed-meshheading:10203697-DNA Fragmentation,
pubmed-meshheading:10203697-Embryo, Mammalian,
pubmed-meshheading:10203697-Fibroblast Growth Factor 2,
pubmed-meshheading:10203697-Gene Expression Regulation,
pubmed-meshheading:10203697-Growth Substances,
pubmed-meshheading:10203697-Hippocampus,
pubmed-meshheading:10203697-Insulin-Like Growth Factor I,
pubmed-meshheading:10203697-Molsidomine,
pubmed-meshheading:10203697-Neurons,
pubmed-meshheading:10203697-Nitric Oxide,
pubmed-meshheading:10203697-Nitric Oxide Donors,
pubmed-meshheading:10203697-Nitroprusside,
pubmed-meshheading:10203697-Oligopeptides,
pubmed-meshheading:10203697-Proto-Oncogene Proteins,
pubmed-meshheading:10203697-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:10203697-Rats,
pubmed-meshheading:10203697-Rats, Sprague-Dawley,
pubmed-meshheading:10203697-Transcription, Genetic,
pubmed-meshheading:10203697-bcl-2-Associated X Protein
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pubmed:year |
1998
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pubmed:articleTitle |
Growth factors prevent changes in Bcl-2 and Bax expression and neuronal apoptosis induced by nitric oxide.
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pubmed:affiliation |
Department of Anatomy and Neuroscience, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan. tama@anat2.med.osaka-u.ac.jp
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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