2026-07-21T11:29:14Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/119662024-09-27T09:40:07Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Cortes-Canteli, Marta
author
Luna-Medina, Rosario
author
Sanz-Sancristobal, Marina
author
Alvarez-Barrientos, Alberto
author
Santos, Angel
author
Perez-Castillo, Ana
funder
Ministerio de Educación y Ciencia (España)
funder
Comunidad de Madrid (España)
funder
Consejo Superior de Investigaciones Científicas (España)
2021-02-22T13:28:01Z
2021-02-22T13:28:01Z
2008-04-15
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
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.
eng
CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury.
journal article
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URL
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CCAATEnhancerBindingProtein_2008.pdf
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025031-figS1.pdf
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CCAATEnhancerBindingProtein_2008.pdf.txt
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025031-figS1.pdf.txt