Abstract
To elucidate further the mechanism of lipid hydroperoxide (LHP) induced neovascularization, we determined the effect of linoleic acid hydroperoxide (18:2-OOH) on bovine aortic endothelial cells (BAEC) in terms of cell proliferation, migration, and tube formation. The influence of some antioxidants on these systems were also investigated. The concentration of basic fibroblast growth factor (bFGF) in the culture medium was determined by an immunoassay. Exposure to 10-7M 18:2-OOH increased BAEC proliferation, migration, and tube formation by 117, 167, and 181%, respectively, as compared with control values. The concentration of bFGF in the culture medium was increased 3 fold by 10-7M 18:2-OOH exposure for 3h, compared with that of controls (5.1 vs. 1.7pg/mg protein). BAEC migration induced by 10-7M 18:2-OOH was inhibited significantly by 10-7M bucillamine (p<0.05), which contains two sulfhydryl groups; by 10-7M troglitazone (p<0.05), which structurally similar to α-tocopherol; and by 10-7M EPC-K1 (p<0.01), an α-tocopherol and ascorbic acid conjugate. Antioxidants showed marginal effects on proliferation. The de novo synthesis of bFGF after the 18:2-OOH stimulus for 3h was reduced from 5.1pg/mg protein to 2.0pg/mg protein by treatment with bucillamine. These results suggest that 18:2-OOH induced BAEC growth is partly related to bFGF release, or synthesis.
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