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- W2022143761 abstract "Down-regulation of peroxisome proliferator-activated receptor α (PPARα) has been proposed to contribute to the progressive deterioration of function during cardiac hypertrophy. However, cellular mechanisms linking PPARα deficiency to cardiac contractile dysfunction remain unknown. We hypothesized that PPARα−/− (KO, n = 20) mice exhibited reduced cardiac performance and that contractile abnormalities were related to oxidative stress. Aged-matched wild type (WT, n = 20) mice were used as controls. Biochemical and mechanical experiments were performed on left ventricle (LV). Data are means ± SEM. Heart/body weight did not differ between groups. Compared to WT, KO had reduced in situ cardiac performance, as assessed by 22% lower echocardiographic fractional shortening. Intrinsic papillary muscle performance was depressed in KO, maximum shortening velocity and isometric tension being respectively 3.5- and 2-fold lower in KO than in WT. Myosin-based velocities, determined by in vitro motility assays, were lower in KO than in WT (1.7 ± 0.1 vs. 1.3 ± 0.2 μm/s, P < 0.05). Myosin isoform composition did not differ between groups. KO exhibited increased nitrosylation staining. Amount of nitrosylated-myosin, the main nitrosylated protein, was higher in KO (1.8 ± 0.2 vs. 1.0 ± 0.3, P < 0.05). Protein modifications related to lipid peroxidation were higher in KO than in WT. MnSOD expression (6.3 ± 0.4 vs. 8.6 ± 0.5, P < 0.05) and activity (3.2 ± 0.2 vs. 6.9 ± 0.4 U/mg) were reduced in KO. Expression and activities of CuZnSOD, catalase, and GPx did not differ between groups. In conclusion, our data showed that lack of PPARα was associated with cardiac dysfunction and identified oxidative damage of myosin as a potential link between PPARα lack and cardiac dysfunction." @default.
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- W2022143761 date "2006-06-01" @default.
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- W2022143761 title "Oxidative stress is involved in cardiac dysfunction of PPARα−/− mice" @default.
- W2022143761 doi "https://doi.org/10.1016/j.yjmcc.2006.03.108" @default.
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