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Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide

Authors

  • Alicia Rubio,

    1. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/Nicolás Cabrera 1, Universidad Autónoma de Madrid, Campus Cantoblanco, Madrid, Spain
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  • José V. Sánchez-Mut,

    1. Cancer Epigenetics and Biology Program, Bellvitge Biomedical Research Institute, Barcelona, Catalonia, Spain
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  • Esther García,

    1. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/Nicolás Cabrera 1, Universidad Autónoma de Madrid, Campus Cantoblanco, Madrid, Spain
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  • Zahady D. Velasquez,

    1. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/Nicolás Cabrera 1, Universidad Autónoma de Madrid, Campus Cantoblanco, Madrid, Spain
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  • Jorge Oliver,

    1. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/Nicolás Cabrera 1, Universidad Autónoma de Madrid, Campus Cantoblanco, Madrid, Spain
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  • Manel Esteller,

    1. Cancer Epigenetics and Biology Program, Bellvitge Biomedical Research Institute, Barcelona, Catalonia, Spain
    2. Institucio Catalana de Recerca i Estudis Avançats, Barcelona, Catalonia, Spain
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  • Jesús Avila

    Corresponding author
    1. Centro de Biología Molecular Severo Ochoa (CSIC-UAM), C/Nicolás Cabrera 1, Universidad Autónoma de Madrid, Campus Cantoblanco, Madrid, Spain
    2. Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), Madrid, Spain
    • Centro de Biología Molecular “Severo Ochoa,” Universidad Autónoma de Madrid, C/Nicolás Cabrera 1, 28049 Madrid, Spain
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Abstract

β Amyloid, present in senile plaques, has been related largely to neuronal loss in the brain of patients with Alzheimer's disease. However, how neurons respond to β amyloid insults is still poorly understood. Here we show that β amyloid increases somatostatin and cortistatin gene expression mainly through an increase in histone 3 lysine 4 methylation (H3K4me3), a modification associated with transcriptional activation. Somatostatin and cortistatin partially decreased β amyloid toxicity in primary cortical neurons in culture. Thus we suggest that neurons respond to β amyloid insults by releasing somatostatin and cortistatin, which will act as a protective agent against β amyloid toxicity. Our results suggest a relevant function for both neuropeptides against β amyloid toxicity, providing new insights into Alzheimer's disease. © 2011 Wiley Periodicals, Inc.

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