Lack of oestrogen protection in amyloid-mediated endothelial damage due to protein nitrotyrosination

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• dc.contributor.author Coma Camprodón, Mireia
• dc.contributor.author Guix Ràfols, Francesc Xavier
• dc.contributor.author Uribesalgo Micàs, Iris
• dc.contributor.author Espuña, G.
• dc.contributor.author Solé, M.
• dc.contributor.author Andreu Martínez, David
• dc.contributor.author Muñoz López, Francisco José, 1964-
• dc.date.accessioned 2024-06-20T14:57:23Z
• dc.date.available 2024-06-20T14:57:23Z
• dc.date.issued 2005
• dc.description.abstract Amyloid beta-peptide (Abeta) cytotoxicity, the hallmark of Alzheimer's disease, implicates oxidative stress in both neurons and vascular cells, particularly endothelial cells. Consequently, antioxidants have shown neuroprotective activities against Abeta-induced cytotoxicity. Among the different antioxidants used in both in vitro and in vivo studies, 17beta-oestradiol (E2) has garnered the most attention. Oestrogen attenuated Abeta(E22Q)-induced toxicity in neurons but failed to protect endothelial cells. Here we show that E2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under Abeta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues. Inhibition of eNOS prevents nitrotyrosination and permits E2-mediated protection against Abeta(E22Q) on endothelial cells. The main nitrotyrosinated proteins in the presence of E2 and Abeta(E22Q) were identified by MALDI-TOF mass spectrometry. These proteins are key players in the regulation of energy production, cytoskeletal integrity, protein metabolism and protection against oxidative stress. Our data highlight the potential damaging consequences of E2 in vascular disorders dealing with oxidative stress conditions, such as cerebral amyloid angiopathy, stroke and ischaemia-reperfusion conditions.
• dc.format.mimetype application/pdf
• dc.identifier.citation Coma M, Guix FX, Uribesalgo I, Espuña G, Solé M, Andreu D, et al. Lack of oestrogen protection in amyloid-mediated endothelial damage due to protein nitrotyrosination. Brain. 2005 Jul;128(Pt 7):1613-21. DOI: 10.1093/brain/awh492
• dc.identifier.doi http://dx.doi.org/10.1093/brain/awh492
• dc.identifier.issn 0006-8950
• dc.identifier.uri http://hdl.handle.net/10230/60549
• dc.language.iso eng
• dc.publisher Oxford University Press
• dc.relation.ispartof Brain. 2005 Jul;128(Pt 7):1613-21
• dc.rights © Oxford University Press. This is a pre-copyedited, author-produced version of an article accepted for publication in Brain: a journal of neurology. following peer review. The version of record Coma M, Guix FX, Uribesalgo I, Espuña G, Solé M, Andreu D, et al. Lack of oestrogen protection in amyloid-mediated endothelial damage due to protein nitrotyrosination. Brain. 2005 Jul;128(Pt 7):1613-21. DOI: 10.1093/brain/awh492 is available online at: 10.1093/brain/awh492
• dc.rights.accessRights info:eu-repo/semantics/openAccess
• dc.subject.keyword Alzheimer’s disease
• dc.subject.keyword Amyloid ß-peptide
• dc.subject.keyword Nitric oxide
• dc.subject.keyword Estrogen
• dc.subject.keyword Nitrotyrosination
• dc.title Lack of oestrogen protection in amyloid-mediated endothelial damage due to protein nitrotyrosination
• dc.type info:eu-repo/semantics/article
• dc.type.version info:eu-repo/semantics/acceptedVersion