Lesioned Low-Density Lipoprotein in Atherosclerotic Apolipoprotein E-Deficient Transgenic Mice and in Humans Is Oxidized and Aggregated
| Autor: | Zvi Adler, Simcha Milo, Victor Kertzman, Tony Hayek, Yaron Bar-El, Michael Aviram, Irit Maor, Shlomo Keidar, J. Oiknine |
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| Rok vydání: | 1995 |
| Předmět: |
Genetically modified mouse
Apolipoprotein E medicine.medical_specialty Arteriosclerosis Biophysics Mice Transgenic Lipoproteins VLDL Biochemistry Mice chemistry.chemical_compound Apolipoproteins E Equivalent Species Specificity Reference Values Internal medicine medicine TBARS Animals Humans Molecular Biology Incubation Aorta Cell Biology Mice Mutant Strains Lipoproteins LDL Endocrinology chemistry Low-density lipoprotein lipids (amino acids peptides and proteins) Lipoproteins HDL Oxidation-Reduction Lipoprotein |
| Zdroj: | Biochemical and Biophysical Research Communications. 216:501-513 |
| ISSN: | 0006-291X |
| DOI: | 10.1006/bbrc.1995.2651 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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