Source:http://linkedlifedata.com/resource/pubmed/id/17916778
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2007-11-27
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pubmed:abstractText |
Nitric oxide has been shown to be an important signaling messenger in ischemic preconditioning (IPC). Accordingly, we investigated whether protein S-nitrosylation occurs in IPC hearts and whether S-nitrosoglutathione (GSNO) elicits similar effects on S-nitrosylation and cardioprotection. Preceding 20 minutes of no-flow ischemia and reperfusion, hearts from C57BL/6J mice were perfused in the Langendorff mode and subjected to the following conditions: (1) control perfusion; (2) IPC; or (3) 0.1 mmol/L GSNO treatment. Compared with control, IPC and GSNO significantly improved postischemic recovery of left ventricular developed pressure and reduced infarct size. IPC and GSNO both significantly increased S-nitrosothiol contents and S-nitrosylation levels of the L-type Ca2+ channel alpha1 subunit in heart membrane fractions. We identified several candidate S-nitrosylated proteins by proteomic analysis following the biotin switch method, including the cardiac sarcoplasmic reticulum Ca2+-ATPase, alpha-ketoglutarate dehydrogenase, and the mitochondrial F1-ATPase alpha1 subunit. The activities of these enzymes were altered in a concentration-dependent manner by GSNO treatment. We further developed a 2D DyLight fluorescence difference gel electrophoresis proteomic method that used DyLight fluors and a modified biotin switch method to identify S-nitrosylated proteins. IPC and GSNO produced a similar pattern of S-nitrosylation modification and cardiac protection against ischemia/reperfusion injury, suggesting that protein S-nitrosylation may play an important cardioprotective role in heart.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1524-4571
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
26
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pubmed:volume |
101
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1155-63
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pubmed:meshHeading |
pubmed-meshheading:17916778-Animals,
pubmed-meshheading:17916778-Biological Transport,
pubmed-meshheading:17916778-Calcium,
pubmed-meshheading:17916778-Cardiotonic Agents,
pubmed-meshheading:17916778-Energy Metabolism,
pubmed-meshheading:17916778-Ischemic Preconditioning, Myocardial,
pubmed-meshheading:17916778-Mice,
pubmed-meshheading:17916778-Mice, Inbred C57BL,
pubmed-meshheading:17916778-Mitochondria,
pubmed-meshheading:17916778-Myocardial Reperfusion Injury,
pubmed-meshheading:17916778-Nitrogen Oxides,
pubmed-meshheading:17916778-Perfusion,
pubmed-meshheading:17916778-Proteins,
pubmed-meshheading:17916778-Ventricular Dysfunction, Left
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pubmed:year |
2007
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pubmed:articleTitle |
Preconditioning results in S-nitrosylation of proteins involved in regulation of mitochondrial energetics and calcium transport.
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pubmed:affiliation |
NHLBI, NIH, Vascular Medicine Branch, Bethesda, MD 20892, USA.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, N.I.H., Extramural,
Research Support, N.I.H., Intramural
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