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First published online April 3, 2008
doi: 10.1242/10.1242/jcs.025031

Journal of Cell Science 121, 1224-1234 (2008)
Published by The Company of Biologists 2008
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Research Article

CCAAT/enhancer binding protein β deficiency provides cerebral protection following excitotoxic injury

Marta Cortes-Canteli1, Rosario Luna-Medina1, Marina Sanz-SanCristobal1, Alberto Alvarez-Barrientos2, Angel Santos3,* and Ana Perez-Castillo1,*

1 Instituto de Investigaciones Biomédicas, Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, Arturo Duperier, 4, and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas (CIBERNED), 28029-Madrid, Spain
2 Centro Nacional de Investigaciones Cardiovasculares, Instituto de Salud Carlos III, Melchor Fernandez Almagro, 3, 28029-Madrid, Spain
3 Departamento de Bioquímica y Biología Molecular, Facultad de Medicina, Universidad Complutense de Madrid, 28040-Madrid, Spain

* Authors for correspondence (e-mails: piedras3{at}med.ucm.es; aperez{at}iib.uam.es)

Accepted 28 January 2008

The CCAAT/enhancer-binding protein β (C/EBPβ, also known as CEBPB) was first identified as a regulator of differentiation and inflammatory processes in adipose tissue and liver. Although C/EBPβ was initially implicated in synaptic plasticity, its function in the brain remains largely unknown. We have previously shown that C/EBPβ regulates the expression of genes involved in inflammatory processes and brain injury. Here, we have demonstrated that the expression of C/EBPβ is notably increased in the hippocampus in a murine model of excitotoxicity. Mice lacking C/EBPβ showed a reduced inflammatory response after kainic acid injection, and exhibited a dramatic reduction in pyramidal cell loss in the CA1 and CA3 subfields of the hippocampus. These data reveal an essential function for C/EBPβ in the pathways leading to excitotoxicity-mediated damage and suggest that inhibitors of this transcription factor should be evaluated as possible neuroprotective therapeutic agents.

Key words: C/EBPβ, Excitotoxicity, Inflammation, Neurodegeneration


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