| Increased expression and altered subcellular distribution of PKC-delta in chronically hypoxic rat myocardium: involvement in cardioprotection. | |
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MedLine Citation:
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PMID: 15576445 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We examined the role of protein kinase C (PKC) in the cardioprotective mechanism induced by long-term adaptation to chronic intermittent hypoxia. Adult male Wistar rats were exposed to hypobaric hypoxia of 7,000 m for 8 h/day, 5 days/wk; the total number of exposures was 24-32. A control group was kept under normoxic conditions. Western blot analysis of PKC isoforms-delta and -epsilon was performed in the cytosol and three particulate fractions of left ventricular myocardium. Infarct size was determined in open-chest animals subjected to 20-min coronary artery occlusion and 3-h reperfusion. The PKC inhibitors chelerythrine (1 or 5 mg/kg) or rottlerin (selective for PKC-delta isoform; 0.3 mg/kg) were administered intravenously as a single bolus 15 min before ischemia. Chronic hypoxia had no effect on the expression and distribution of PKC-epsilon. The relative amount of PKC-delta increased in the cytosol and nuclear-cytoskeletal, mitochondrial, and microsomal fractions of chronically hypoxic myocardium by 100%, 212%, 237%, and 146%, respectively, compared with corresponding normoxic values. Chronic hypoxia decreased the size of myocardial infarction (normalized to the area at risk) by about one-third on the average (P < 0.05). Both doses of chelerythrine tended to reduce infarction in controls, and only the high dose completely abolished the improvement of ischemic tolerance in hypoxic hearts (P < 0.05). Rottlerin attenuated the infarct size-limiting effect of chronic hypoxia (P < 0.05), and it had no effect in controls. These results suggest that chronic intermittent hypoxia-induced cardioprotection in rats is partially mediated by PKC-delta; the contribution of other isoforms remains to be determined. |
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Authors:
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Jan Neckár; Irena Marková; Frantisek Novák; Olga Nováková; Ondrej Szárszoi; Bohuslav Ost'ádal; Frantisek Kolár |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2004-12-02 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 288 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2005 Apr |
Date Detail:
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Created Date: 2005-03-17 Completed Date: 2005-04-20 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1566-72 Citation Subset: IM |
Affiliation:
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Institute of Physiology, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia / metabolism* Blood Pressure Chronic Disease Enzyme Inhibitors / pharmacology Heart Rate Heart Ventricles / enzymology Hematocrit Male Myocardial Infarction / metabolism* Myocardial Reperfusion Injury / metabolism* Myocardium / enzymology* Protein Kinase C / antagonists & inhibitors, metabolism* Protein Kinase C-delta Protein Kinase C-epsilon Rats Rats, Wistar |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; EC 2.7.1.-/Prkcd protein, rat; EC 2.7.1.-/Prkce protein, rat; EC 2.7.11.13/Protein Kinase C; EC 2.7.11.13/Protein Kinase C-delta; EC 2.7.11.13/Protein Kinase C-epsilon |
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