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Epigenetic control of somatostatin and cortistatin expression by β amyloid peptide

2011; Wiley; Volume: 90; Issue: 1 Linguagem: Inglês

10.1002/jnr.22731

1097-4547

Alicia Rubio, José V. Sánchez‐Mut, Esther García, Zahady D. Velásquez, Jorge Oliver‐De La Cruz, Manel Esteller, Jesús Ávila,

Epigenetics and DNA Methylation

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.