Neuroprotective effects of EpoL against oxidative stress induced by soluble oligomers of Aβ peptide
Entity
UAM. Departamento de Farmacología; UAM. Instituto Teófilo Hernando de I+D del Medicamento (ITH)Publisher
Elsevier B.V.Date
2019-04-02Citation
10.1016/j.redox.2019.101187
Redox Biology 24 (2019): 101187
ISSN
2213-2317DOI
10.1016/j.redox.2019.101187Funded by
Grant Innova-Corfo “13IDL2-18688”; Conicyt Grant “Beca Doctorado Nacional no. 21130386”; Fondecyt Grant “1161078”Editor's Version
https://doi.org/10.1016/j.redox.2019.101187Subjects
Alzheimer disease; Amyloid beta; Erythropoietin; Glycosylation; Neuroprotection; Oxidative stress; FarmaciaRights
© 2019 Published by Elsevier B.V.Esta obra está bajo una licencia de Creative Commons Reconocimiento-NoComercial-SinObraDerivada 4.0 Internacional.
Abstract
Erythropoietin is a glycoproteic hormone that regulates hematopoiesis by acting on its specific receptor (EpoR). The expression of EpoR in the central nervous system (CNS) suggests a role for this hormone in the brain. Recently, we developed a new Epo variant without hematopoietic activity called EpoL, which showed marked neuroprotective effects against oxidative stress in brain ischemia related models. In this study, we have evaluated the neuroprotective effects of EpoL against oxidative stress induced by chronic treatment with Aβ. Our results show that EpoL was neuroprotective against Aβ-induced toxicity by a mechanism that implicates EpoR, reduction in reactive oxygen species, and reduction in astrogliosis. Furthermore, EpoL treatment improved calcium handling and SV2 levels. Interestingly, the neuroprotective effect of EpoL against oxidative stress induced by chronic Aβ treatment was achieved at a concentration 10 times lower than that of Epo. In conclusion, EpoL, a new variant of Epo without hematopoietic activity, is of potential interest for the treatment of diseases related to oxidative stress in the CNS such as Alzheimer disease.
Files in this item
Google Scholar:Castillo, C.
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Fernández-Mendívil, C.
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Buendia, I.
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Saavedra, P.
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Meza, C.
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Parra, N. C.
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López, M. G.
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Toledo, J. R.
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Fuentealba, J.
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