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oai:repisalud.isciii.es:20.500.12105/119662024-09-27T09:40:07Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Cortes-Canteli, Marta author Luna-Medina, Rosario author Sanz-Sancristobal, Marina author Alvarez-Barrientos, Alberto author Santos, Angel author Perez-Castillo, Ana author 2008-04-15 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. J Cell Sci. 2008; 121(Pt 8):1224-34 10.1242/jcs.025031 0021-9533 Journal of cell science 18388310 http://hdl.handle.net/20.500.12105/11966 CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury.