title: Expression of C/EBPalpha and C/EBPbeta in glial cells in vitro after inducing glial activation by different stimuli.
abstract: We studied the involvement of two members of the CCAAT/enhancer binding proteins (C/EBPs) family of transcription factors, C/EBPalpha and C/EBPbeta, in glial activation induced by different stimuli in rat cerebellar neuronal-glial cultures. Glial activation was induced by two types of neuronal death--excitotoxic and apoptotic. We had previously reported that these two induction mechanisms resulted in different patterns of glial activation (K. Pérez-Capote, J. Serratosa, C. Solà, Excitotoxic and apoptotic neuronal death induce different patterns of glial activation in vitro, J. Neurochem. 94 (2005) 226-237), only the former involving an inflammatory response. Glial activation was also induced by lipopolysaccharide (LPS) from E. coli, an inflammatory agent with a known direct effect on glial cells. Using immunocytochemical techniques, here we examined whether changes in C/EBPalpha and C/EBPbeta expression are selectively associated with a determinate pattern of glial activation. Excitotoxic neuronal death increased glial C/EBPbeta expression in the absence of alterations in C/EBPalpha expression, while no effect was observed following neuronal apoptosis. LPS treatment decreased C/EBPalpha and increased C/EBPbeta expression in glial cells. These results implicate C/EBPs in glial activation, although these two factors appear to have different roles. C/EBPalpha expression decreases only in response to LPS, while C/EBPbeta expression is increased by both LPS and excitotoxic neuronal death, although not by neuronal apoptosis. These results show that C/EBPbeta plays an active role in glial activation, but only when this involves an inflammatory reaction, suggesting a role for C/EBPbeta in neuroinflammation.
authors.affiliation: Department of Pharmacology and Toxicology, Institut d'Investigacions Biomèdiques de Barcelona-Consejo Superior de Investigaciones Científicas, Institut d'Investigacions Biomèdiques August Pi i Sunyer, Barcelona, Spain.
authors.forename: Kamil
authors.initials: K
authors.lastname: Pérez-Capote
authors.forename: Josep
authors.initials: J
authors.lastname: Saura
authors.forename: Joan
authors.initials: J
authors.lastname: Serratosa
authors.forename: Carme
authors.initials: C
authors.lastname: Solà
mesh_terms: D000818:Animals; D022763:CCAAT-Enhancer-Binding Protein-alpha / Q000378:metabolism*; D022782:CCAAT-Enhancer-Binding Protein-beta / Q000378:metabolism*; D016923:Cell Death / Q000187:drug effects; D002478:Cells, Cultured; D002531:Cerebellum / Q000166:cytology; D015870:Gene Expression / Q000502:physiology*; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry / Q000379:methods; D008070:Lipopolysaccharides / Q000494:pharmacology; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D051381:Rats
chemical_list: D022763:CCAAT-Enhancer-Binding Protein-alpha; D022782:CCAAT-Enhancer-Binding Protein-beta; D005904:Glial Fibrillary Acidic Protein; D008070:Lipopolysaccharides