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

Abstract:

:The CCAAT/enhancer-binding protein beta (C/EBPbeta, also known as CEBPB) was first identified as a regulator of differentiation and inflammatory processes in adipose tissue and liver. Although C/EBPbeta was initially implicated in synaptic plasticity, its function in the brain remains largely unknown. We have previously shown that C/EBPbeta regulates the expression of genes involved in inflammatory processes and brain injury. Here, we have demonstrated that the expression of C/EBPbeta is notably increased in the hippocampus in a murine model of excitotoxicity. Mice lacking C/EBPbeta 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/EBPbeta in the pathways leading to excitotoxicity-mediated damage and suggest that inhibitors of this transcription factor should be evaluated as possible neuroprotective therapeutic agents.

journal_name

J Cell Sci

journal_title

Journal of cell science

authors

Cortes-Canteli M,Luna-Medina R,Sanz-Sancristobal M,Alvarez-Barrientos A,Santos A,Perez-Castillo A

doi

10.1242/jcs.025031

subject

Has Abstract

pub_date

2008-04-15 00:00:00

pages

1224-34

issue

Pt 8

eissn

0021-9533

issn

1477-9137

pii

121/8/1224

journal_volume

121

pub_type

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