2024-03-29T14:01:24Zhttp://repisalud.isciii.es/oai/requestoai:repisalud.isciii.es:20.500.12105/119662023-09-28T13:41:59Zcom_20.500.12105_2145com_20.500.12105_2051com_20.500.12105_2144col_20.500.12105_2146
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
0021-9533
http://hdl.handle.net/20.500.12105/11966
18388310
10.1242/jcs.025031
Journal of cell science
CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury.