Angiogenic effect of lipid hydroperoxide on bovine aortic endothelial cells

To elucidate further the mechanism of lipid hydroperoxide (LHP) induced neo vascularization, we determined the effect of linoleic acid hydroperoxide (1 8:2-OOH) on bovine aortic endothelial cells (BAEC) in terms of cell prolife ration, migration, and tube formation. The influence of some antioxidants o n these systems were also investigated. The concentration of basic fibrobla st growth factor (bFGF) in the culture medium was determined by an immunoas say. Exposure to 10(-7) M 18:2-OOH increased BAEC proliferation, migration, and tube formation by 117, 167, and 181%, respectively, as compared with c ontrol values. The concentration of bFGF in the culture medium was increase d 3 fold by 10(-7) M 18:2-OOH exposure for 3 h, compared with that of contr ols (5.1 vs. 1.7 pg/mg protein). BAEC migration induced by 10(-7) M 18:2-OO H was inhibited significantly by 10(-7) M bucillamine (p < 0.05), which con tains two sulfhydryl groups; by 10(-7) M troglitazone (p < 0.05), which str ucturally similar to alpha-tocopherol; and by 10(-7) M EPC-KI (p < 0.01), a n alpha-tocopherol and ascorbic acid conjugate. Antioxidants showed margina l effects on proliferation. The de novo synthesis of bFGF after the 18:2-OO H stimulus for 3 h was reduced from 5.1 pg/mg protein to 2.0 pg/mg protein by treatment with bucillamine. These results suggest that 18:2-OOH induced BAEC growth is partly related to bFGF release, or synthesis.