TY - JOUR
T1 - Endothelial cell monolayer dysfunction caused by oxidized low density lipoprotein
T2 - Attenuation by oleic acid
AU - Karman, R. J.
AU - Garcia, J. G.N.
AU - Hart, C. M.
N1 - Funding Information:
The authors gratefully acknowledge the technical assistance of Shehnaz Kahn and the assistance of Ms Marla Mahem in the preparation of this manuscript. This work was supported by a National Institute of Health Training Grant HL07774 (R. J. IO; by HL50533 and 44746 (J. G. N. G.); by Research Gram (R6-033-N) from the American Lung Association (C. M. H.), by a Grant-in-Aid (93007440) from the American Heart Association (C. M. H), and by the Research Service of the Veterans Affairs Medical Center (J. G. N. G. and C. M. H.).
PY - 1997/5
Y1 - 1997/5
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0030920358&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030920358&partnerID=8YFLogxK
U2 - 10.1016/S0952-3278(97)90582-2
DO - 10.1016/S0952-3278(97)90582-2
M3 - Article
C2 - 9175170
AN - SCOPUS:0030920358
SN - 0952-3278
VL - 56
SP - 345
EP - 353
JO - Prostaglandins Leukotrienes and Essential Fatty Acids
JF - Prostaglandins Leukotrienes and Essential Fatty Acids
IS - 5
ER -