Oleic acid (18:1) may exert beneficial effects on the pathogenesis of vascular disease by a variety of mechanisms. To determine if 18:1 exerts direct protective effects on vascular endothelial cells, porcine pulmonary artery endothelial cells (PAEC) were supplemented with 0.1 mM 18:1, γ-linolenic acid (18:3), or ethanol vehicle (ETOH) prior to treatment with low density lipoprotein (LDL), or Cu2+-oxidized (LDL (OXLDL). Treatment with neither LDL nor OXLDL (100 μg protein/ml) for 24-48 h caused PAEC cytotoxicity, whereas OXLDL, but not (LDL, caused derangements in PAEC actin microfilament architecture and monolayer barrier dysfunction. Supplementation with 18:1, but not 18:3, attenuated derangements caused by OXLDL and lysophosphatidylcholine, a component of OXLDL. These results demonstrate that monounsaturated fatty acids directly alter the response of vascular endothelial cells to OXLDL and may retard the atherosclerotic process by decreasing the efflux of macromolecules (e.g. (LDL) into the vessel wall.
|Original language||English (US)|
|Number of pages||9|
|Journal||Prostaglandins Leukotrienes and Essential Fatty Acids|
|State||Published - May 1997|
ASJC Scopus subject areas
- Clinical Biochemistry
- Cell Biology