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Complement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ
Elena Hernandez-Encinas1,2, Diana Aguilar-Morante1,3, Jose A Morales-Garcia1,2
1Instituto de Investigaciones Biomédicas, (CSIC-UAM), Arturo Duperier, 4, 28029, Madrid, Spain.
Insights
CCAAT/enhancer-binding protein β (C/EBPβ) regulates complement component 3 (C3) in the hippocampus. This suggests C/EBPβ may influence brain disorders involving excitotoxicity and inflammation via C3.
Area of Science:
- Neuroscience
- Molecular Biology
- Immunology
Background:
- CCAAT/enhancer-binding protein β (C/EBPβ) is a transcription factor involved in inflammation and proliferation.
- C/EBPβ plays a role in brain injury and inflammatory processes.
- Complement component 3 (C3) is a downstream target of C/EBPβ and may mediate its pro-inflammatory effects in neural cells.
Purpose of the Study:
- To investigate the role of C/EBPβ in regulating C3 expression in the hippocampus following excitotoxic injury.
- To determine if C/EBPβ directly influences C3 expression in vivo.
Main Methods:
- Utilized C/EBPβ knockout mice and wild-type littermates.
- Administered kainic acid to induce excitotoxic injury in the hippocampus.
- Analyzed hippocampal brain slices for the co-expression of C/EBPβ and C3.
Main Results:
- C/EBPβ and C3 were found to co-express in the CA1 and CA3 regions of the hippocampus after injury.
- Mice lacking C/EBPβ showed significantly reduced C3 expression following kainic acid injection.
- These findings indicate that C/EBPβ regulates C3 expression in the hippocampus in vivo.
Conclusions:
- CCAAT/enhancer-binding protein β (C/EBPβ) plays a role in regulating C3 expression in the hippocampus.
- C/EBPβ may contribute to brain disorders involving excitotoxic and inflammatory processes through C3 regulation.
Background:
The 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.
Methods:
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.
Results:
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.
Conclusions:
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.
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