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Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine

Title
Superoxide is a potential culprit of caspase-3 dependent endothelial cell death induced by lysophosphatidylcholine
Authors
Park S.Kim J.A.Choi S.Suh S.H.
Ewha Authors
서석효박성희
SCOPUS Author ID
서석효scopus; 박성희scopus
Issue Date
2010
Journal Title
Journal of Physiology and Pharmacology
ISSN
0867-5910JCR Link
Citation
vol. 61, no. 4, pp. 375 - 381
Indexed
SCIE; SCOPUS WOS scopus
Abstract
Oxidative stress in the vascular wall has intimately been implicated in the apoptosis of human umbilical vein endothelial cells (HUVECs) by lysophosphatidylcholine (LPC). However, the major type of reactive oxygen species (ROS) in this apoptotic signaling pathway remains to be clarified. In this study, we report that superoxide mediate LPC-induced caspase-3 dependent apoptosis in cultured HUVECs. The stimulation of HUVECs with LPC evoked apoptosis and ROS generation, and inhibited nitric oxide (NO) production in a dose-dependent manner. The classical caspase-3 dependent apoptosis was determined after 16 hours treatment by Western blotting using an antibody against cleaved caspase-3. The caspase-3 activation induced by LPC was prominently inhibited by antioxidants or NO donors and enhanced by NO inhibitors. Especially, LPC-induced caspase-3 activation was inhibited by superoxide dismutase (SOD) and enhanced by ammonium tetrathiomolybdate, SOD inhibitor. Additionally, xanthine/xanthine oxidase mixture increased the caspase-3 activation but catalase failed to reduce this superoxide-induced caspase-3 activation. These findings indicate that the superoxide generation caused by LPC activates the caspase-3 which results in HUVECs death. This study reveals some evidences linking superoxide with caspase-3 activation and provides a new dimension to superoxidemediated caspase-3 activation in developing the endothelial dysfunction and atherosclerosis.
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의학전문대학원 > 의학과 > Journal papers
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