Affiliations: Institute of Biochemistry, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Correspondence:
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Corresponding author: Ana Cristina Carvalho Rego, PhD, Institute of Biochemistry, Faculty of Medicine and Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal. Tel.: +39 351 239 820190; Fax: +39 351 239 822776; E-mail: acrego@cnc.cj.uc.pt.
Abstract: In this study we analysed the effect of Bcl-2 on the cytotoxicity induced by the amyloid-β (Aβ25–35) and prion (PrP106–126) peptides by using GT1-7 puro and GT1-7 bcl-2 (overexpressing the anti-apoptotic protein Bcl-2) neural cells. Exposure to Aβ25–35 (1–5 μM) and PrP106–126 (25 μM) caused a decrease in cell viability, as determined by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. These data were correlated with Aβ25–35 and PrP106–126-induced activation of caspase-9, which is linked to the mitochondrial death pathway, and the activation of the effector caspase-3, suggesting cell death by apoptosis. Furthermore, Bcl-2 overexpression protected from loss of cell viability and caspase-9 and -3 activation induced by Aβ25–35 and PrP106–126, showing that Bcl-2 is neuroprotective against apoptotic cell death caused by amyloidogenic peptides.
