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Dadun > Depósito Académico > CIMA (Centro de Investigación Médica Aplicada) > Área de Neurociencias > Neurofarmacología y conducta > DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista >

Enhanced expression of the voltage-dependent anion channel 1 (VDAC1) in Alzheimer's disease transgenic mice: an insight into the pathogenic effects of amyloid-β
Authors: Cuadrado-Tejedor, M. (Mar)
Vilariño, M. (Marcos)
Cabodevilla, F. (Felipe)
Rio, J. (Joaquín) del
Frechilla, D. (Diana)
Perez-Mediavilla, L.A. (Luis Alberto)
Keywords: Alzheimer’s disease
amyloid-beta
hexokinase I
phospho-VDAC1
voltage-dependent anion channel 1 (VDAC1)
Issue Date: 2011
Publisher: IOS Press
Publisher version: http://dx.doi.org/10.3233/JAD-2010-100966
ISSN: 1387-2877 (Print);1875-8908 (Online)
Citation: Cuadrado-Tejedor M, Vilariño M, Cabodevilla F, Del Rio J, Frechilla D, Perez-Mediavilla A. "Enhanced expression of the voltage-dependent anion channel 1 (VDAC1) in Alzheimer's disease transgenic mice: an insight into the pathogenic effects of amyloid-β". J Alzheimers Dis. 2011 23(2):195-206.
Abstract
The mitochondrial voltage-dependent anion channel 1 (VDAC1) is involved in the release of apoptotic proteins with possible relevance in Alzheimer's disease (AD) neuropathology. Through proteomic analysis followed by Western blotting and immunohistochemical techniques, we have found that VDAC1 is overexpressed in the hippocampus from amyloidogenic AD transgenic mice models. VDAC1 was also overexpressed in postmortem brain tissue from AD patients at an advanced stage of the disease. Interestingly, amyloid-β (Aβ) soluble oligomers were able to induce upregulation of VDAC1 in a human neuroblastoma cell line, further supporting a correlation between Aβ levels and VDAC1 expression. In hippocampal extracts from transgenic mice, a significant increase was observed in the levels of VDAC1 phosphorylated at an epitope that is susceptible to phosphorylation by glycogen synthase kinase-3β, whose activity was also increased. The levels of hexokinase I (HXKI), which interacts with VDAC1 and affects its function, were decreased in mitochondrial samples from AD models. Since phospho-VDAC and reduced HXKI levels favors a VDAC1 conformational state more prone to the release proapoptotic factors, regulation of the function of this channel may be a promising therapeutic approach to combat AD.
Permanent link: http://hdl.handle.net/10171/19472
Appears in Collections:DA - CIMA - Neurociencias - Neurofarmacología y conducta - Artículos de Revista
DA - Ciencias - Bioquímica y Biología molecular - Artículos de Revista

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