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Effects of Recombinant Adenovirus-Mediated Uncoupling Protein 2 Overexpression on Endothelial Function and Apoptosis

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Author(s)
송대규이인규
Alternative Author(s)
Song, Dae KyuLee, In Kyu
Publication Year
2005
Abstract
—Increased oxidative stress in vascular cells plays a key role in the development of endothelial dysfunction and
atherosclerosis. Uncoupling protein 2 (UCP2) is an important regulator of intracellular reactive oxygen species (ROS)
production. This study was undertaken to test the hypothesis that, UCP2 functions as an inhibitor of the atherosclerotic
process in endothelial cells. Adenovirus-mediated UCP2 (Ad-UCP2) overexpression led to a significant increase in
endothelial nitric oxide synthase (eNOS) and decrease in endothelin-1 mRNA expression in human aortic endothelial
cells (HAECs). Moreover, UCP2 inhibited the increase in ROS production and NF- B activation, and apoptosis of
HAECs induced by lysophophatidylcholine (LPC) and linoleic acid. LPC and linoleic acid caused mitochondrial
calcium accumulation and transient mitochondrial membrane hyperpolarization, which was followed by depolarization.
UCP2 overexpression prevented these processes. In isolated rat aorta, Ad-UCP2 infection markedly improved impaired
vascular relaxation induced by LPC. The data collectively suggest that UCP2, functions as a physiologic regulator of
ROS generation in endothelial cells. Thus, measures to increase UCP2 expression in vascular endothelial cells may aid
in preventing the development and progression of atherosclerosis in patients with metabolic syndrome. (Circ Res. 2005;
96:1200-1207.)
Key Words: endothelial cells uncoupling protein oxidative stress vascular endothelial function apoptosis
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