ECE2007 Poster Presentations (1) (659 abstracts)
Effects of PGC-1α on endothelial function and apoptosis
Joong-Yeol Park 1 , Jong Chul Won 1 , Ki-Up Lee 1 , Woo Je Lee 2 , Kyung Soo Ko 2 , Kee-Ho Song 3 & In-Kyu Lee 4
1University of Ulsan College of Medicine, Seoul, South Korea; 2Inje University College of Medicine, Seoul, South Korea; 3Konkuk University School of Medicine, Seoul, South Korea; 4Kyungpook National University, Daegu, South Korea.
Aims: Central obesity is associated with increased cardiovascular morbidity and mortality. It has been proposed that increased lipid accumulation in vascular tissue and the consequent increase in oxidative stress may be a missing link between obesity and atherosclerosis. The peroxisome proliferators-activated receptor (PPAR)-γ coactivator 1-α (PGC-1α) is a transcriptional coactivator playing an important role in energy metabolism. PGC-1α is present in vascular cells, but its role in vascular endothelial cells has not been established. In this study, we examined the effect of adenoviral overexpression of PGC-1α (Ad-PGC-1α) in human aortic endothelial cells (HAECs) on apoptosis induced by linoleic acid (LA).
Methods: Effect of PGC-1 on HAECs apoptosis was evaluated by ELISA, WST-1 assay, and caspase activity. Using Ad-PGC-1 and ANT-1 siRNA, effect of PGC-1 and ANT-1 on reactive oxygen species (ROS) production, fatty acid oxidation (FAO) and mitochondrial membrane potential (Δψm) were analyzed.
Results: PGC-1α prevented LA-induced endothelial apoptosis. PGC-1α also reduced LA-induced increases of antioxidant enzyme expression and ROS accumulation at basal state. LA decreased the activity of adenosine nucleotide translocase (ANT), and increased Δψm. In the Ad-PGC-1α-infected HAECs, activity and the mRNA expression of ANT-1 were increased and LA did not increase Δψm. siRNA against ANT-1 reversed the changes induced by PGC-1α.
Conclusion: These data suggest that PGC-1α functions as a physiologic regulator of ROS generation in endothelial cells and that part of this effect is mediated by ANT-dependent increase in FAO.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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