English   español  
Please use this identifier to cite or link to this item: http://hdl.handle.net/10261/122830
logo share SHARE logo core CORE   Add this article to your Mendeley library MendeleyBASE

Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL
Exportar a otros formatos:


CCAAT/enhancer binding protein β directly regulates the expression of the complement component 3 gene in neural cells: implications for the pro-inflammatory effects of this transcription factor

AuthorsHernandez-Encinas, Elena; Aguilar Morante, Diana ; Cortés-Canteli, Marta ; Morales-García, José A. ; Giné, Elena; Santos, Ángel; Pérez Castillo, Ana
Neural cells
Transcriptional regulation
Issue Date2015
PublisherBioMed Central
CitationJournal of Neuroinflammation 12: 14 (2015)
Abstract[Background]: The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor, which was first identified as a regulator of differentiation and inflammatory processes mainly in adipose tissue and liver; however, its function in the brain was largely unknown for many years. Previous studies from our laboratory indicated that C/EBPβ is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. [Methods]: We first performed cDNA microarrays analysis using hippocampal RNA isolated from C/EBPβ+/+ and C/EBPβ−/− mice. Immunocytochemical and immunohistochemical studies were done to evaluate C/EBPβ and C3 levels. Transient transfection experiments were made to analyze transcriptional regulation of C3 by C/EBPβ. To knockdown C/EBPβ and C3 expression, mouse astrocytes were infected with lentiviral particles expressing an shRNA specific for C/EBPβ or an siRNA specific for C3. [Results]: Among the genes displaying significant changes in expression was complement component 3 (C3), which showed a dramatic decrease in mRNA content in the hippocampus of C/EBPβ−/− mice. C3 is the central component of the complement and is implicated in different brain disorders. In this work we have found that C/EBPβ regulates C3 levels in rodents glial in vitro and in the rat Substantia nigra pars compacta (SNpc) in vivo following an inflammatory insult. Analysis of the mouse C3 promoter showed that it is directly regulated by C/EBPβ through a C/EBPβ consensus site located at position −616/-599 of the gene. In addition, we show that depletion of C/EBPβ by a specific shRNA results in a significant decrease in the levels of C3 together with a reduction in the increased levels of pro-inflammatory agents elicited by lipopolysaccharide treatment. [Conclusions]: Altogether, these results indicate that C3 is a downstream target of C/EBPβ, and it could be a mediator of the pro-inflammatory effects of this transcription factor in neural cells.
DescriptionThis is an Open Access article distributed under the terms of the Creative Commons Attribution License.
Publisher version (URL)http://dx.doi.org/10.1186/s12974-014-0223-2
Appears in Collections:(IIBM) Artículos
Files in This Item:
File Description SizeFormat 
CCAATenhancer.pdf1,94 MBAdobe PDFThumbnail
Show full item record
Review this work

Related articles:

WARNING: Items in Digital.CSIC are protected by copyright, with all rights reserved, unless otherwise indicated.