Lesioned low density lipoprotein in atherosclerotic apolipoprotein E-deficient transgenic mice and in humans is oxidized and aggregated.
We analyzed lesioned LDL in both atherosclerotic humans and in the apo E deficient (E degree) mice and compared its characteristics to plasma LDL. Lesioned LDL, in comparison to plasma LDL, was minimally oxidized and aggregated. Upon incubation of E degree-aortic lesions with 125[I]-labeled LDL, a time-dependent oxidation of the lipoprotein occurred as evident by a rapid and substantial elevation in LDL-associated TBARS from 0.2 to 10.3 and 14.5 nmoles of MDA equivalents/mg LDL protein after 2 and 24 hours of incubation, respectively. Only minimal LDL aggregates could be detected after 2 hours of incubation. Extensive LDL aggregation (15%), however, occurred after 24 h of incubation. Similar results were obtained on using human lesioned aortas. We conclude that both oxidation and aggregation of lesioned LDL could be the result of aortic lesioned-induced modification of the lipoprotein, and both of these modified forms of LDL can further contribute to the acceleration of the atherosclerotic process.
D000818:Animals; D001011:Aorta / Q000473:pathology*; D001057:Apolipoproteins E / Q000172:deficiency*; D001161:Arteriosclerosis / Q000097:blood* / Q000473:pathology*; D006801:Humans; D008075:Lipoproteins, HDL / Q000097:blood / Q000302:isolation & purification; D008077:Lipoproteins, LDL / Q000032:analysis* / Q000097:blood / Q000302:isolation & purification; D008079:Lipoproteins, VLDL / Q000097:blood / Q000302:isolation & purification; D051379:Mice; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D010084:Oxidation-Reduction; D012016:Reference Values; D013045:Species Specificity
D001057:Apolipoproteins E; D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D008079:Lipoproteins, VLDL