| First Author | Cortes-Canteli M | Year | 2008 |
| Journal | J Cell Sci | Volume | 121 |
| Issue | Pt 8 | Pages | 1224-34 |
| PubMed ID | 18388310 | Mgi Jnum | J:139594 |
| Mgi Id | MGI:3808947 | Doi | 10.1242/jcs.025031 |
| Citation | Cortes-Canteli M, et al. (2008) CCAAT/enhancer binding protein beta deficiency provides cerebral protection following excitotoxic injury. J Cell Sci 121(Pt 8):1224-34 |
| abstractText | 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. |
