Oxidative protein damage in cells engaged in beta-amyloidosis is related to apoE genotype |
| |
Authors: | Mazur-Kolecka Bozena Frackowiak Janusz Kowal Dagmar Krzeslowska Jolanta Dickson Dennis |
| |
Institution: | New York State Institute for Basic Research in Developmental Disabilities, Department of Pathological Neurobiology, 1050 Forest Hill Rd, Staten Island, NY 10314, USA. |
| |
Abstract: | The epsilon4 allele of apolipoprotein E (apoE) is a risk factor for Alzheimer's disease. The reduced antioxidant defense in epsilon4 carriers is suggested to contribute to beta-amyloidosis. We found that oxidative stress induced by treatment with Fe2+ ions raised more protein carbonyls in vascular smooth muscle cells isolated from human brains with apoE genotype epsilon4/epsilon4 than with 3epsilon/epsilon3 and epsilon3/epsilon4. Antioxidant vitamin E prevented formation of carbonyls but not in cells with genotype epsilon4/epsilon4. Treatment with Fe2+ ions induced cellular accumulation of amyloid-beta protein (Abeta)-immunoreactive material that co-localized with heme oxygenase, a marker of oxidative stress, and apoE. We hypothesize that the damage caused by oxidation in epsilon4/epsilon4 carriers facilitates development of beta-amyloidosis. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|