Oxidized low-density lipoproteins delay endothelial wound healing: lack of effect of vitamin E

• Published in: Annals of nutrition and metabolism 1995-01, Vol.39 (1), p.1-8
• Main Authors: Boissonneault, G.A, Wang, Y, Chung, B.H
• Format: Article
• Language: English
• Subjects: albumins; Animals; Biological and medical sciences; cell growth; Cell metabolism, cell oxidation; Cell physiology; Cells, Cultured; DNA - biosynthesis; dose response; endothelium; Endothelium, Vascular - injuries; Endothelium, Vascular - metabolism; Fundamental and applied biological sciences. Psychology; healing; in vitro culture; Linoleic Acid; linoleic acid hydroperoxide; Linoleic Acids - pharmacology; Lipid Peroxides - pharmacology; Lipoproteins, LDL - pharmacology; low density lipoprotein; Molecular and cellular biology; Original Paper; oxidation; Oxidation-Reduction; Serum Albumin - metabolism; Swine; transfer; vitamin E; Vitamin E - pharmacology; vitamin supplements; Wound Healing - drug effects
• ISSN: 0250-6807; 1421-9697
• DOI: 10.1159/000177836

The purpose of this study was to examine the influence of oxidized low-density lipoprotein (oxLDL) on endothelial regrowth in an in vitro wounding model and the possible protection afforded by vitamin E (E). Endothelial cells grown on micropore filters were wounded by scraping and allowed to reestablish growth on denuded areas in the presence of LDL or oxLDL (25-200 micrograms/ml), linoleic acid (FA, 90 micromolar) or linoleic acid hydroperoxide (OFA, 15 micromolar) for 24 h. Some monolayers were pretreated with 25 micromolar E for 24 h. Transendothelial albumin movement was used as a measure of endothelial barrier function and as an indicator of endothelial monolayer regrowth. Exposure to levels of oxLDL as low as 25 micrograms/ml for 24 h resulted in depressed endothelial monolayer regrowth, whereas native LDL was without effect and pre-enrichment with 25 micromolar E offered no protection. In comparison, E preenrichment improved endothelial regrowth to control levels in FA- and OFA-treated cultures, unlike oxLDL-treated cultures. It is concluded that circulating oxLDL may reduce regrowth of wounded endothelium and supplemental E may not offer protection. Moreover, fatty acids or their hydroperoxides are unlikely to be involved in this effect.