OXIDIZED LOW-DENSITY LIPOPROTEINS DELAY ENDOTHELIAL WOUND-HEALING - LACK OF EFFECT OF VITAMIN-E

被引:16
作者
BOISSONNEAULT, GA
WANG, Y
CHUNG, BH
机构
[1] UNIV KENTUCKY,MULTIDISCIPLINARY PHD PROGRAM NUTR SCI,LEXINGTON,KY 40536
[2] UNIV ALABAMA,DEPT MED,BIRMINGHAM,AL 35294
关键词
ENDOTHELIAL CELLS; ENDOTHELIAL CELL INJURY; VITAMIN-E; OXIDIZED LIPOPROTEINS; CELL PROLIFERATION; CELL MIGRATION;
D O I
10.1159/000177836
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 mu g/ml), linoleic acid (FA, 90 mu M) or linoleic acid hydroperoxide (OFA, 15 mu M) for 24 h. Some monolayers were pretreated with 25 mu ME 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 mu g/ml for 24 h resulted in depressed endothelial monolayer regrowth, whereas native LDL was without effect and preenrichment with 25 mu M 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.
引用
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页码:1 / 8
页数:8
相关论文
共 34 条
[1]  
Witztum J.L., The role of oxidized LDL in atherosclerosis’, Hypercholesterolemia, Hypo- Cholesterolcmia, Hypertriglyceridemia, pp. 353-365, (1990)
[2]  
Yla-Herttuala S., Palinski W., Rosen-Feld M.E., Parthasarathy S., Carew T.E., Butler S., Witztum J.L., Steinberg D., Evidence for the presence of oxidatively modified low density lipoprotein in atherosclerotic lesions of rabbit and man, J Clin Invest, 84, pp. 1086-1095, (1989)
[3]  
Boyd H.C., Gown A.M., Wolfbauer G., Chait A., Direct evidence for a protein recognized by a monoclonal antibody against oxidatively modified LDL in atherosclerotic lesions from a Watanabe heritable hyperlipide- mic rabbit, Am J Pathol, 135, pp. 815-825, (1989)
[4]  
Esterbauer H., Dieber-Rotheneder M., Striegl G., Wacg G., Role of vitamin E in preventing the oxidation of low-density lipoprotein, Am J Clin Nutr, 53, pp. 314S-321S, (1991)
[5]  
Sato K., Niki E., Shimasaki H., Free radical-mediated chain oxidation of low density lipoprotein and its synergistic inhibition by vitamin E and vitamin C, Arch Biochem Bio- Phvs, 279, pp. 402-405, (1990)
[6]  
Rcaven P.D., Parthasarathy S., Beltz W.F., Witztum J.L., Effect of probucol dosage on plasma lipid and lipoprotein levels and on protection of low density lipoprotein against
[7]  
n vitro oxidation in humans, Arterioscler Thromb, 12, pp. 318-324, (1992)
[8]  
Morel D.W., Chisolm G.M., Antioxidant treatment of diabetic rats inhibits lipoprotein oxidation and cytotoxicity, J Lipid Res, 30, pp. 1827-1834, (1989)
[9]  
Nagano Y., Nakamura T., Matsuza-Wa Y., Cho M., Ueda Y., Kita T., Probucol and atherosclerosis in the Watanabe heritable hyperlipidemic rabbit - Long-term antiatherogenic effect and effects on established plaques, Atherosclerosis, 92, pp. 131-140, (1992)
[10]  
Williams R.J., Motteram J.M., Sharp C.H., Gallagher P.J., Dietary vitamin E and the attenuation of early lesion development in modified Watanabe rabbits, Atherosclerosis, 94, pp. 153-159, (1992)