ENDOTHELIAL-CELL MONOLAYER DYSFUNCTION CAUSED BY OXIDIZED LOW-DENSITY-LIPOPROTEIN - ATTENUATION BY OLEIC-ACID

Oleic acid (18:1) may exert beneficial effects on the pathogenesis of vascular disease by a variety of mechanisms. To determine if 18:1 exer ts direct protective effects on vascular endothelial cells, porcine pu lmonary artery endothelial cells (PAEC) were supplemented with 0.1 mM 18:1, gamma-linolenic acid (18:3), or ethanol vehicle (ETOH) prior to treatment with low density lipoprotein (LDL), or Cu2+-oxidized LDL (OX LDL). Treatment with neither LDL nor OXLDL (100 mu g protein/ml) for 2 4-48 h caused PAEC cytotoxicity, whereas OXLDL, but not LDL, caused de rangements in PAEC actin microfilament architecture and monolayer barr ier dysfunction. Supplementation with 18:1, but not 18:3, attenuated d erangements caused by OXLDL and lysophosphatidylcholine, a component o f OXLDL. These results demonstrate that monounsaturated fatty acids di rectly alter the response of vascular endothelial cells to OXLDL and m ay retard the atherosclerotic process by decreasing the efflux of macr omolecules (e.g. LDL) into the vessel wall.