Bcl-2 Overexpression Protects Against Amyloid-Beta and Prion Toxicity in GT1-7 Neural Cells
Titel:
Bcl-2 Overexpression Protects Against Amyloid-Beta and Prion Toxicity in GT1-7 Neural Cells
Auteur:
Ferreiro, Elisabete Eufrásio, Ana Pereira, Cláudia Oliveira, Catarina R. Rego, A. Cristina
Verschenen in:
Journal of Alzheimer's disease
Paginering:
Jaargang 12 (2007) nr. 3 pagina's 223-228
Jaar:
2007-11-26
Inhoud:
In this study we analysed the effect of Bcl-2 on the cytotoxicity induced by the amyloid-β (Aβ_{25-35}) and prion (PrP_{106-126}) peptides by using GT1-7 puro and GT1-7 bcl-2 (overexpressing the anti-apoptotic protein Bcl-2) neural cells. Exposure to Aβ _{25-35} (1–5 μM) and PrP_{106-126} (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 Aβ_{25-35} and PrP_{106-126}-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 Aβ_{25-35} and PrP_{106-126}, showing that Bcl-2 is neuroprotective against apoptotic cell death caused by amyloidogenic peptides.