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This Article Full Text Full Text (PDF) All Versions of this Article: 288/4/H1566    most recent 00586.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (12) Citing Articles via Google Scholar Google Scholar Articles by Neckár, J. Articles by Kolár, F. Search for Related Content PubMed PubMed Citation Articles by Neckár, J. Articles by Kolár, F.

Increased expression and altered subcellular distribution of PKC- in chronically hypoxic rat myocardium: involvement in cardioprotection

Jan Necká,¹ Irena Marková,² Frantiek Novák,² Olga Nováková,² Ondrej Szárszoi,¹ Bohuslav Ot'ádal,¹ and Frantiek Kolá¹

¹Institute of Physiology, Academy of Sciences of the Czech Republic and Centre for Experimental Cardiovascular Research, ²Faculty of Science, Charles University, Prague, Czech Republic

Submitted 14 June 2004 ; accepted in final form 24 November 2004

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- and - 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- 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-. The relative amount of PKC- 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-; the contribution of other isoforms remains to be determined.

ischemia-reperfusion; infarct size; protein kinase C

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