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Research Article Free access | 10.1172/JCI3531

Oxidized LDL activates fas-mediated endothelial cell apoptosis.

M Sata and K Walsh

Division of Cardiovascular Research, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA.

Find articles by Sata, M. in: JCI | PubMed | Google Scholar

Division of Cardiovascular Research, St. Elizabeth's Medical Center, Tufts University School of Medicine, Boston, Massachusetts 02135, USA.

Find articles by Walsh, K. in: JCI | PubMed | Google Scholar

Published November 1, 1998 - More info

Published in Volume 102, Issue 9 on November 1, 1998
J Clin Invest. 1998;102(9):1682–1689. https://doi.org/10.1172/JCI3531.
© 1998 The American Society for Clinical Investigation
Published November 1, 1998 - Version history
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Abstract

Oxidized low density lipoproteins (OxLDL) promote chronic inflammatory responses in the vasculature that give rise to atherosclerotic plaques. Fas ligand (FasL) is naturally expressed on the vascular endothelium where it can induce apoptosis in Fas-expressing immune cells as they enter the vessel wall. Although vascular endothelial cells are normally resistant to Fas-mediated cell death, OxLDL were shown to induce apoptosis in cultured endothelial cells and endothelium of arterial explants by a process that could be inhibited with Fas L neutralizing antibodies. OxLDL-induced cell death was also reduced in the aortic endothelium cultured from gld (FasL-/-) and lpr (Fas-/-) mice as compared with wild-type mice. OxLDL acted by sensitizing endothelial cells to death signals from the Fas receptor. Thus, the ability of OxLDL to promote Fas-mediated endothelial cell suicide may be a feature that contributes to their atherogenicity.

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  • Version 1 (November 1, 1998): No description

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