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- W1963865712 abstract "The aim was to determine the expression and subcellular distribution of PKC isoforms δ and ɛ in the left ventricular myocardium of normoxic and chronically hypoxic rats and to examine acute effects of PKC inhibitors. Adult male Wistar rats were either exposed for 5 weeks to intermittent hypobaric hypoxia of 7000 m (8 h/day, 5 days/week) or kept under normoxic conditions. After this period, both hypoxic and normoxic rats were divided into three subgroups: chelerythrine-treated (5 mg/kg), rottlerin-treated (0.3 mg/kg) and untreated controls. Hearts were collected 15 min after the intravenous administration of the respective PKC inhibitor. The formation of nitrotyrosine, as a marker of nitrosative stress, was enhanced in chronically hypoxic myocardium (immunofluorescent staining). Chronic hypoxia increased the protein expression of PKCδ in nuclear-cytoskeletal (1000 ×g), mitochondrial (8000 ×g), microsomal (100000 ×g), and cytosolic fractions by 83%, 88%, 90%, and 59%, respectively, as determined by Western blotting. PKCδ-selective inhibitor rottlerin partially reversed the hypoxia-induced increase in PKCδ abundance in the mitochondrial fraction by 34%. Quantitative analysis of ventricular frozen sections following immunofluorescent staining revealed similar changes in the distribution of this isoform. In contrast, the expression of PKCɛ was decreased in the microsomal fraction (by 40%) from chronically hypoxic myocardium. Chelerythrine, general PKC inhibitor, had no effect on the expression and distribution of any PKC isoform. These results support and extend our earlier findings regarding the involvement of nitric oxide and PKCδ in myocardial adaptation to chronic hypoxia." @default.
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- W1963865712 date "2008-04-01" @default.
- W1963865712 modified "2023-10-16" @default.
- W1963865712 title "Protein kinase C isoforms in chronically hypoxic rat heart" @default.
- W1963865712 doi "https://doi.org/10.1016/j.yjmcc.2008.02.167" @default.
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