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Overexpression of Human Superoxide Dismutase Inhibits Oxidation of Low-Density Lipoprotein by Endothelial Cells
Journal article   Open access   Peer reviewed

Overexpression of Human Superoxide Dismutase Inhibits Oxidation of Low-Density Lipoprotein by Endothelial Cells

Xiang Fang, Neal L Weintraub, C. David Rios, David A Chappell, Ralf M Zwacka, John F Engelhardt, Larry W Oberley, Tao Yan, Donald D Heistad and Arthur A Spector
Circulation research, Vol.82(12), pp.1289-1297
06/29/1998
DOI: 10.1161/01.RES.82.12.1289
PMID: 9648725
url
https://doi.org/10.1161/01.RES.82.12.1289View
Published (Version of record) Open Access

Abstract

Oxidation of LDL in the subendothelial space has been proposed to play a key role in atherosclerosis. Endothelial cells produce superoxide anions (O (2) sup [center dot] -) and oxidize LDL in vitro; however, the role of O2 sup [center dot] - in endothelial cell-induced LDL oxidation is unclear. Incubation of human LDL (200 [micro sign]g/mL) with bovine aortic endothelial cells (BAECs) for 18 hours resulted in a 4-fold increase in LDL oxidation compared with cell-free incubation (22.5 +/- 1.1 versus 6.3 +/- 0.2 [mean +/- SEM] nmol malondialdehyde/mg LDL protein, respectively; P<0.05). Under similar conditions, incubation of LDL with porcine aortic endothelial cells resulted in a 5-fold increase in LDL oxidation. Inclusion of exogenous copper/zinc superoxide dismutase (Cu/ZnSOD, 100 [micro sign]g/mL) in the medium reduced BAEC-induced LDL oxidation by 79%. To determine whether the intracellular SOD content can have a similar protective effect, BAECs were infected with adenoviral vectors containing cDNA for human Cu/ZnSOD (AdCu/ZnSOD) or manganese SOD (AdMnSOD). Adenoviral infection increased the content and activity of either Cu/ZnSOD or MnSOD in the cells and reduced cellular O2 sup [center dot] - release by two thirds. When cells infected with AdCu/ZnSOD or AdMnSOD were incubated with LDL, formation of malondialdehyde was decreased by 77% and 32%, respectively. Two other indices of LDL oxidation, formation of conjugated dienes and increased LDL electrophoretic mobility, were similarly reduced by SOD transduction. These data suggest that production of O2 sup [center dot] - contributes to endothelial cell-induced oxidation of LDL in vitro. Furthermore, adenovirus-mediated transfer of cDNA for human SOD, particularly Cu/ZnSOD, effectively reduces oxidation of LDL by endothelial cells. (Circ Res. 1998;82:1289-1297.)

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