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


, : Lack of oestrogen protection in amyloid-mediated endothelial damage due to protein nitrotyrosination. Brain 128(Pt 7): 1613-1621

Amyloid beta-peptide (A beta) 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 A beta-induced cytotoxicity. Among the different antioxidants used in both in vitro and in vivo studies, 17 beta-oestradiol (E-2) has garnered the most attention. Oestrogen attenuated A beta(E22Q)-induced toxicity in neurons but failed to protect endothelial cells. Here we show that E-2-mediated activation of endothelial nitric oxide synthase (eNOS) increases the production of nitric oxide (NO), which, under A beta(E22Q)-induced oxidative damage, results in the formation of peroxynitrite and increased nitration of tyrosine residues. Inhibition of eNOS prevents nitrotyrosination and permits E-2-mediated protection against A beta(E22Q) on endothelial cells. The main nitrotyrosinated proteins in the presence of E-2 and A beta(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 E-2 in vascular disorders dealing with oxidative stress conditions, such as cerebral amyloid angiopathy, stroke and ischaemia-reperfusion conditions.

US$19.90

PMID: 15817516

DOI: 10.1093/brain/awh492


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