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Vitamin E but not 17B-estradiol protect against vascular toxicity induced by B-amyloid wild type and the Dutch amyploid variant

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dc.contributor.author Muñoz López, Francisco José, 1964-
dc.contributor.author Opazo, Carlos M.
dc.contributor.author Gil Gómez, Gabriel
dc.contributor.author Tapia, Gladys
dc.contributor.author Fernández, Virginia
dc.contributor.author Valverde, M. A. (Miguel Ángel), 1963-
dc.contributor.author Inestrosa, Nibaldo C.
dc.date.accessioned 2012-07-05T06:54:12Z
dc.date.available 2012-07-05T06:54:12Z
dc.date.issued 2002
dc.identifier.citation Muñoz FJ, Opazo C, Gil-Gómez G, Tapia G, Fernández V, Valverde MA et al. Vitamin E but not 17B-estradiol protect against vascular toxicity induced by B-amyloid wild type and the Dutch amyploid variant. J. Neurosci. 2002;22(8):3081-89. DOI: 10.1523/jneurosci.22-08-03081.2002
dc.identifier.issn 0270-6474
dc.identifier.uri http://hdl.handle.net/10230/16666
dc.description.abstract Amyloid β-peptide (Aβ) fibril deposition on cerebral vessels produces cerebral amyloid angiopathy that appears in the majority of Alzheimer's disease patients. An early onset of a cerebral amyloid angiopathy variant called hereditary cerebral hemorrhage with amyloidosis of the Dutch type is caused by a point mutation in Aβ yielding AβGlu22→Gln. The present study addresses the effect of amyloid fibrils from both wild-type and mutated Aβ on vascular cells, as well as the putative protective role of antioxidants on amyloid angiopathy. For this purpose, we studied the cytotoxicity induced by Aβ1–40 Glu22→Gln and Aβ1–40 wild-type fibrils on human venule endothelial cells and rat aorta smooth muscle cells. We observed that AβGlu22→Gln fibrils are more toxic for vascular cells than the wild-type fibrils. We also evaluated the cytotoxicity of Aβ fibrils bound with acetylcholinesterase (AChE), a common component of amyloid deposits. Aβ1–40 wild-type–AChE fibrillar complexes, similar to neuronal cells, resulted in an increased toxicity on vascular cells. Previous reports showing that antioxidants are able to reduce the toxicity of Aβ fibrils on neuronal cells prompted us to test the effect of vitamin E, vitamin C, and 17β-estradiol on vascular damage induced by Aβwild-type and AβGlu22→Gln. Our data indicate that vitamin E attenuated significantly the Aβ-mediated cytotoxicity on vascular cells, although 17β-estradiol and vitamin C failed to inhibit the cytotoxicity induced by Aβ fibrils.
dc.format.mimetype application/pdf
dc.language.iso eng
dc.publisher Society for Neuroscience
dc.relation.ispartof Journal of Neuroscience. 2002;22(8):3081-89
dc.rights © 2002, Society for Neuroscience. The published version is available at: http://www.jneurosci.org/content/22/8/3081
dc.subject.other Alzheimer, Malaltia d' -- Fisiologia patològica
dc.subject.other Proteïna beta-amiloide
dc.subject.other Estrès oxidatiu -- Fisiologia patològica
dc.title Vitamin E but not 17B-estradiol protect against vascular toxicity induced by B-amyloid wild type and the Dutch amyploid variant
dc.type info:eu-repo/semantics/article
dc.identifier.doi http://dx.doi.org/10.1523/jneurosci.22-08-03081.2002
dc.subject.keyword Alzheimer’s disease
dc.subject.keyword CAA
dc.subject.keyword HCHWA-D
dc.subject.keyword Amyloid
dc.subject.keyword Vitamin E
dc.subject.keyword 17B-estradiol
dc.subject.keyword Vitamin C
dc.subject.keyword Oxidative stress
dc.subject.keyword Acetylcholinesterase
dc.subject.keyword Endothelial cells
dc.subject.keyword Vascular smooth muscle cells
dc.rights.accessRights info:eu-repo/semantics/openAccess
dc.type.version info:eu-repo/semantics/publishedVersion

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