Hernandez-Encinas, ElenaAguilar-Morante, DianaMorales-Garcia, Jose AGine, ElenaSanz-SanCristobal, MarinaSantos, AngelPerez-Castillo, Ana2023-01-252023-01-252016-10-21http://hdl.handle.net/10668/10553The CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor implicated in the control of proliferation, differentiation, and inflammatory processes mainly in adipose tissue and liver; although more recent results have revealed an important role for this transcription factor in the brain. Previous studies from our laboratory indicated that CCAAT/enhancer-binding protein β is implicated in inflammatory process and brain injury, since mice lacking this gene were less susceptible to kainic acid-induced injury. More recently, we have shown that the complement component 3 gene (C3) is a downstream target of CCAAT/enhancer-binding protein β and it could be a mediator of the proinflammatory effects of this transcription factor in neural cells. Adult male Wistar rats (8-12 weeks old) were used throughout the study. C/EBPβ+/+ and C/EBPβ-/- mice were generated from heterozygous breeding pairs. Animals were injected or not with kainic acid, brains removed, and brain slices containing the hippocampus analyzed for the expression of both CCAAT/enhancer-binding protein β and C3. In the present work, we have further extended these studies and show that CCAAT/enhancer-binding protein β and C3 co-express in the CA1 and CA3 regions of the hippocampus after an excitotoxic injury. Studies using CCAAT/enhancer-binding protein β knockout mice demonstrate a marked reduction in C3 expression after kainic acid injection in these animals, suggesting that indeed this protein is regulated by C/EBPβ in the hippocampus in vivo. Altogether these results suggest that CCAAT/enhancer-binding protein β could regulate brain disorders, in which excitotoxic and inflammatory processes are involved, at least in part through the direct regulation of C3.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/C/EBPβC3ExcitotoxicityNeurodegenerationNeuroinflammationAnimalsCCAAT-Enhancer-Binding Protein-betaCD11b AntigenComplement C3Disease Models, AnimalExcitatory Amino Acid AgonistsFluoresceinsGene Expression RegulationGlial Fibrillary Acidic ProteinHippocampusInterleukin-1betaKainic AcidMaleMiceMice, TransgenicNerve DegenerationNeurogliaRNA, MessengerRatsRats, WistarComplement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ.research article27769255open access10.1186/s12974-016-0742-01742-2094PMC5073972https://doi.org/10.1186/s12974-016-0742-0https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5073972/pdf