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Copper and cell‐oxidized low‐density lipoprotein induces activator protein 1 in fibroblasts, endothelial and smooth muscle cells
Author(s) -
Mazière Cécile,
Djavaheri-Mergny Mojgan,
Frey-Fressart Véronique,
Delattre Jacques,
Mazière Jean-Claude
Publication year - 1997
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(97)00545-0
Subject(s) - lipid peroxidation , chemistry , cycloheximide , ap 1 transcription factor , low density lipoprotein , biochemistry , oxidative stress , reactive oxygen species , lipoprotein , activator (genetics) , microbiology and biotechnology , biology , protein biosynthesis , transcription factor , cholesterol , gene
The effect of cupric ion‐ or endothelial cell‐oxidized low‐density lipoproteins (LDL) on transcription factor AP1 activation was investigated by electrophoretic mobility shift assay. Both oxidized LDL induced AP1 activation in fibroblasts, endothelial and smooth muscle cells. This phenomenon was also observed in the presence of cycloheximide. α‐Tocopherol, a lipophilic free radical scavenger, and N ‐acetylcysteine, an hydrophilic antioxidant, partially inhibited the stimulatory effect of Cu 2+ ‐oxidized LDL. LDL modified by the mixture of the oxygen radicals OH· and O 2 · − , which generated lipid peroxidation products, also initiated AP1 activation, whereas LDL modified by OH· alone, which did not lead to marked LDL lipid peroxidation, was ineffective. Thus, lipid peroxidation products seem at least partially involved in the activation mechanism. Since AP1 activity is essential for the regulation of genes involved in cell growth and differentiation, our study suggests that the oxidative stress induced by oxidized LDL might be related to the fibroproliferative response observed in the atherosclerotic plaque.