Concentration Polarization of Oxidative Modification of Low-Density Lipoproteins: Its Effect on Oxidative Modification of Low-Density Lipoprotein Uptake and Apoptosis of the Endothelial Cells

ASAIO Journal ◽  
2010 ◽  
Vol 56 (5) ◽  
pp. 468-474 ◽  
Author(s):  
Zufeng Ding ◽  
Yubo Fan ◽  
Xiaoyan Deng
1985 ◽  
Vol 79 (1) ◽  
pp. 317-325
Author(s):  
J. Gaffney ◽  
D. West ◽  
F. Arnold ◽  
A. Sattar ◽  
S. Kumar

Acetylated low density lipoprotein (Ac-LDL) is taken up by bovine aortic and adrenal capillary cells but not by brain capillary cells. This indicates that the uptake of Ac-LDL is not a feature of all types of endothelial cell. A quantitative examination of lipoprotein uptake by flow cytometry showed cells in G2M took up 45% more Ac-LDL than those in G1S. Compared with confluent cultures, sub-confluent bovine aortic cells took up three times as much LDL but Ac-LDL uptake was increased by only 34%. This indicates that the Ac-LDL receptor is not down-regulated to the same extent as that for LDL.


1998 ◽  
Vol 336 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Cécile MAZIÈRE ◽  
Françoise DANTIN ◽  
Marie-Alix CONTE ◽  
James DEGONVILLE ◽  
Dany ALI ◽  
...  

Oxidative modification of low-density lipoprotein (LDL) is an important feature in the initiation and progression of atherosclerosis. LDL modification by endothelial cells was studied after supplementation of the cells with oleic acid and polyunsaturated fatty acids (PUFA) of the n-6 and n-3 series. In terms of the lipid peroxidation product [thiobarbituric acid reactive substances (TBARS)] content and diene level of the LDL particle, oleic acid had no significant effect, and linoleic acid was poorly effective. Gamma linolenic acid (C18:3, n-6) and arachidonic acid (C20:4, n-6) increased by about 1.6–1.9-fold the cell-mediated LDL modification. PUFA from the n-3 series, alpha linolenic acid (C18:3, n-3), eicosapentaenoic acid (C20:5, n-3) and docosahexaenoic acid (C22:6, n-3), induced a less marked effect (1.3–1.6-fold increase). The relative electrophoretic mobility of the LDL particle and its degradation by macrophages were enhanced in parallel. Concomitantly, PUFA stimulated superoxide anion secretion by endothelial cells. The intracellular TBARS content was also increased by PUFA. Comparison of PUFA from the two series indicates a good correlation between LDL oxidative modification, superoxide anion secretion and intracellular lipid peroxidation. The lipophilic antioxidant vitamin E decreased the basal as well as the PUFA-stimulated LDL peroxidation. These results indicate that PUFAs with a high degree of unsaturation of the n-6 and n-3 series could accelerate cell-mediated LDL peroxidation and thus aggravate the atherosclerotic process.


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