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Superoxide generated by lysophosphatidylcholine induces endothelial nitric oxide synthase downregulation in human endothelial cells

Title
Superoxide generated by lysophosphatidylcholine induces endothelial nitric oxide synthase downregulation in human endothelial cells
Authors
Choi S.Park S.Liang G.H.Kim J.A.Suh S.H.
Ewha Authors
서석효최신규박성희
SCOPUS Author ID
서석효scopus; 최신규scopus; 박성희scopus
Issue Date
2010
Journal Title
Cellular Physiology and Biochemistry
ISSN
1015-8987JCR Link
Citation
vol. 25, no. 41308, pp. 233 - 240
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
We examined the mechanism through which lysophosphatidylcholine (LPC) induces endothelial nitric oxide (eNOS) downregulation. Human umbilical vein endothelial cells (HUVECs) were treated with LPC (50-150 μM) for 0.5-2 h or the reactive oxygen species (ROS) donors, xanthine/xanthine oxidase (X/XO), 1,4-hydroquinone (HQ) or tert-butylhydroperoxide (TBHP) for 2 h. Protein levels of eNOS, superoxide dismutase1 (SOD1), catalase, and phospho-extracellular signal regulated kinase 1/2 (pERK 1/2) were assessed using immunoblotting. LPC treatment reduced SOD1 levels but increased catalase levels. The superoxide donors X/XO and HQ showed similar effects. The hydroperoxide donor TBHP increased SOD1 levels but did not change catalase levels. LPC concentration-and time-dependently decreased eNOS levels, but this effect was blocked by antioxidants and SOD and potentiated by the SOD1 inhibitor, ammonium tetrathiomolybdate. LPC and X/XO inhibited ERK1/2 phosphorylation, whereas TBHP stimulated phosphorylation. Taken together, these data indicate that LPC induces superoxide overload in HUVECs via SOD1 inhibition and downregulates phospho-ERK1/2 and eNOS levels. Copyright © 2010 S. Karger AG, Basel.
DOI
10.1159/000276557
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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