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Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide
Author(s) -
Rubio Alicia,
SánchezMut José V.,
García Esther,
Velasquez Zahady D.,
Oliver Jorge,
Esteller Manel,
Avila Jesús
Publication year - 2012
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.22731
Subject(s) - somatostatin , epigenetics , amyloid (mycology) , neuropeptide , h3k4me3 , senile plaques , neuroscience , alzheimer's disease , toxicity , biology , gene expression , medicine , microbiology and biotechnology , gene , disease , biochemistry , receptor , promoter , botany
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.