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• W2140892017 abstract "Objective: Activation of peroxisome proliferator-activated receptor α (PPARα) and PPARγ plays beneficial roles in cardiovascular disorders such as atherosclerosis and heart reperfusion. Although PPARα and γ have been documented to reduce oxidative stress in the vasculature and the heart, the role of PPARδ remains poorly studied. Methods and results: We focused on PPARδ function in the regulation of oxidative stress-induced apoptosis in the rat cardiomyoblast cell line H9c2. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we showed that PPARδ is the predominantly expressed isotype whereas PPARα was weakly detected. By performing cell viability assays, we also showed that the selective PPARδ agonist GW501516 protected cells from H2O2-induced cell death. The protective effect of GW501516 was due to an inhibition of H2O2-triggered apoptosis as shown by annexin-V labeling, DNA fragmentation analysis, and caspase-3 activity measurement. We demonstrated by transient transfection of a dominant negative mutant of PPARδ that the protection induced by GW501516 was totally dependent on PPARδ. Semi-quantitative RT-PCR and Western blotting analysis demonstrated that GW501516 treatment upregulated catalase. Moreover, forced overexpression of catalase inhibited H2O2-triggered apoptosis, as evidenced by annexin-V labeling. Conclusion: Taken together, our results account for an important role of PPARδ in inhibiting the onset of oxidative stress-induced apoptosis in H9c2 cells. PPARδ appears to be a new therapeutic target for the regulation of heart reperfusion-associated oxidative stress and stimulation of enzymatic antioxidative defences." @default.
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• W2140892017 date "2006-02-01" @default.
• W2140892017 modified "2023-09-27" @default.
• W2140892017 title "Peroxisome proliferator-activated receptor δ (PPARδ) activation protects H9c2 cardiomyoblasts from oxidative stress-induced apoptosis" @default.
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• W2140892017 doi "https://doi.org/10.1016/j.cardiores.2005.10.019" @default.
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