Source:http://linkedlifedata.com/resource/pubmed/id/15497042
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2004-10-21
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pubmed:abstractText |
In order to understand the intracellular mechanism of preconditioning, we investigated the relationship among activities of extracellular signal-regulated protein kinases (ERKs), the expression of hypoxia-inducible factor -1alpha (HIF-1alpha) and the effect of hypoxic preconditioning (HPC) on cell injury induced by hypoxia-reoxygenation in cultured neonatal rat cardiomyocytes 24 h after brief hypoxia. Cultured cardiomyocytes of neonatal Sprague-Dawley rats were divided into four groups: hypoxia/reoxygenation (H/R), hypoxia preconditioning (HPC), hypoxia preconditioning + mitogen-activated protein kinase (MAPK) inhibitor PD98059 (HPC+PD98059), and control (C). We measured the survival rate and apoptosis rate of cardiomyocytes at 6 or 12 h after hypoxia/reoxygenation, activities of extracellular signal-regulated protein kinases (ERKs), and expression of hypoxia-inducible factor-1alpha (HIF-1alpha). We found that the survival rate of cardiomyocytes in hypoxic preconditioning group increased by 6.08% and 7.91% at 6 and 12 h after hypoxia/reoxygenation (n=6, P<0.05), respectively, and the apoptotic rate decreased by 10.92% and 14.34% (n=6, P<0.05) respectively. Hypoxic preconditioning increased the abundance of phospho-ERK1/2 by 3-folds and expression of HIF-1alpha by 1-fold in whole cell extracts from hypoxic preconditioned cardiomyocytes. PD98059, an inhibitor of the upstream kinase of ERKs, abolished the anti-injury effect, ERKs activation, and expression of HIF-1alpha induced by hypoxic preconditioning. Statistical analysis indicated that there was negative correlation between apoptotic rate and activities of ERKs or expression of HIF-1alpha, and positive correlation between activities of ERKs and expression of HIF-1alpha. It is concluded that hypoxic preconditioning protects cardiomyocytes from hypoxia/reoxygenation-induced injury and that upregulation of HIF-1alpha through ERKs pathway mediates the cardioprotection of hypoxic preconditioning.
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pubmed:language |
chi
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Extracellular Signal-Regulated MAP...,
http://linkedlifedata.com/resource/pubmed/chemical/Hif1a protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoxia-Inducible Factor 1,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoxia-Inducible Factor 1, alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0371-0874
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
25
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pubmed:volume |
56
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
609-14
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:15497042-Animals,
pubmed-meshheading:15497042-Animals, Newborn,
pubmed-meshheading:15497042-Apoptosis,
pubmed-meshheading:15497042-Cell Hypoxia,
pubmed-meshheading:15497042-Cell Survival,
pubmed-meshheading:15497042-Cells, Cultured,
pubmed-meshheading:15497042-DNA-Binding Proteins,
pubmed-meshheading:15497042-Extracellular Signal-Regulated MAP Kinases,
pubmed-meshheading:15497042-Hypoxia-Inducible Factor 1,
pubmed-meshheading:15497042-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:15497042-Ischemic Preconditioning, Myocardial,
pubmed-meshheading:15497042-Myocytes, Cardiac,
pubmed-meshheading:15497042-Nuclear Proteins,
pubmed-meshheading:15497042-Rats,
pubmed-meshheading:15497042-Rats, Sprague-Dawley,
pubmed-meshheading:15497042-Transcription Factors
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pubmed:year |
2004
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pubmed:articleTitle |
[Role of hypoxia-inducible factor-1alpha in the prevention of cardiomyocyte injury induced by hypoxic preconditioning].
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pubmed:affiliation |
Department of Pathophysiology, Chinese PLA General Hospital, Beijing, China.
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pubmed:publicationType |
Journal Article,
English Abstract,
Research Support, Non-U.S. Gov't
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