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Título

Effect of the Alzheimer amyloid fragment Aβ(25-35) on Akt/PKB kinase and survival of PC12 cells

AutorMartín, Daniel CSIC ORCID; Salinas, Marta; López-Valdaliso, Raquel; Serrano, Elena CSIC; Recuero, María CSIC; Cuadrado, Antonio CSIC ORCID
Fecha de publicación2001
EditorWiley-Blackwell
CitaciónJournal of Neurochemistry 78(5): 1000-1008 (2001)
ResumenThe phosphatidylinositol 3 kinase (PI3K)-Akt/PKB pathway protects neurons from apoptosis caused by diverse stress stimuli. However, its protective role against the amyloid beta peptide (Aβ), a major constituent of Alzheimer's disease plaques, has not been studied. We investigated the effect of the Aβ-derived Aβ(25-35) peptide on apoptosis and on the Akt survival pathway in PC12 cells. Cells submitted to micromolar concentrations of Aβ(25-35) exhibited increased production of reactive oxygen species (ROS) and morphological alterations consistent with apoptosis. Akt1 was activated shortly after incubation with Aβ(25-35) and Aβ(1-40) with a kinetics different to that of nerve-derived growth factor. Akt1 activation was blocked by the PI3K inhibitor wortmannin. We tested the hypothesis that Akt1 might modify the vulnerability of neural cells to apoptosis induced by Aβ(25-35). Overexpression of an active version of Akt1 attenuated the apoptotic effect of Aβ(25-35) as determined by flow cytometry. Moreover, PC12 cells overexpressing a membrane-targeted N-myristylated fusion protein of enhanced green fluorescence protein (EGFP) and mouse Akt1 exhibited lower levels of ROS than control EGFP-transfected cells. The present findings demonstrate that Akt1 is activated in response to Aβ(25-35) in a PI3K-dependent manner and that active Akt1 protects PC12 cells against the pro-apoptotic action of this peptide.
URIhttp://hdl.handle.net/10261/79908
DOI10.1046/j.1471-4159.2001.00472.x
Identificadoresdoi: 10.1046/j.1471-4159.2001.00472.x
issn: 0022-3042
e-issn: 1471-4159
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