| Granulocyte colony-stimulating factor mediates cardioprotection against ischemia/reperfusion injury via phosphatidylinositol-3-kinase/Akt pathway in canine hearts. | |
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MedLine Citation:
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PMID: 16775664 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Recent studies suggest that G-CSF prevents cardiac remodeling following myocardial infarction (MI) likely through regeneration of the myocardium and coronary vessels. However, it remains unclear whether G-CSF administered at the onset of reperfusion prevents ischemia/reperfusion injury in the acute phase. We investigated acute effects of G-CSF on myocardial infarct size and the incidence of lethal arrhythmia and evaluated the involvement of the phosphatidylinositol-3 kinase (PI3K) in the in vivo canine models. METHODS: In open-chest dogs, left anterior descending coronary artery (LAD) was occluded for 90 minutes followed by 6 hours of reperfusion. We intravenously administered G-CSF (0.33 micro/kg/min) for 30 minutes from the onset of reperfusion. Wortmannin, a PI3K inhibitor, was selectively administered into the LAD after the onset of reperfusion. RESULTS: G-CSF significantly (p<0.05) reduced myocardial infarct size (38.7+/-4.3% to 15.7+/-5.3%) and the incidence of ventricular fibrillation during reperfusion periods (50% to 0%) compared with the control. G-CSF enhanced Akt phospholylation in ischemic canine myocardium. Wortmannin blunted both the infarct size-limiting and anti-arrhythmic effects of G-CSF. G-CSF did not change myeloperoxidase activity, a marker of neutrophil accumulation, in the infarcted myocardium. CONCLUSION: An intravenous administration of G-CSF at the onset of reperfusion attenuates ischemia/reperfusion injury through PI3K/Akt pathway in the in vivo model. G-CSF administration can be a promising candidate for the adjunctive therapy for patients with acute myocardial infarction. |
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Authors:
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Hiroyuki Takahama; Tetsuo Minamino; Akio Hirata; Akiko Ogai; Hiroshi Asanuma; Masashi Fujita; Masakatsu Wakeno; Osamu Tsukamoto; Ken-ichiro Okada; Kazuo Komamura; Seiji Takashima; Yoshiro Shinozaki; Hidezo Mori; Naoki Mochizuki; Masafumi Kitakaze |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cardiovascular drugs and therapy / sponsored by the International Society of Cardiovascular Pharmacotherapy Volume: 20 ISSN: 0920-3206 ISO Abbreviation: Cardiovasc Drugs Ther Publication Date: 2006 Jun |
Date Detail:
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Created Date: 2006-07-20 Completed Date: 2006-11-27 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 8712220 Medline TA: Cardiovasc Drugs Ther Country: United States |
Other Details:
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Languages: eng Pagination: 159-65 Citation Subset: IM |
Affiliation:
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Department of Cardiovascular Medicine, National Cardiovascular Center, Suita, Osaka, Japan. |
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| MeSH Terms | |
Descriptor/Qualifier:
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1-Phosphatidylinositol 3-Kinase
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physiology* Animals Dogs Granulocyte Colony-Stimulating Factor / therapeutic use* Myocardial Infarction / drug therapy* Myocardial Reperfusion Injury / prevention & control* Myocardium / metabolism Peroxidase / metabolism Proto-Oncogene Proteins c-akt / physiology* Ventricular Fibrillation / drug therapy |
| Chemical | |
Reg. No./Substance:
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143011-72-7/Granulocyte Colony-Stimulating Factor; EC 1.11.1.7/Peroxidase; EC 2.7.1.137/1-Phosphatidylinositol 3-Kinase; EC 2.7.11.1/Proto-Oncogene Proteins c-akt |
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