ArticleJournal of neuroinflammation2016
Complement component 3 (C3) expression in the hippocampus after excitotoxic injury: role of C/EBPβ.
Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- C/EBPβ Drives Ischemia-Induced Microglial Inflammatory Reprogramming Through Transcriptional Activation of ATF3 and Exacerbates Brain Injury.Molecular neurobiology · 2026Article
- Riluzole shifts glial responses to protect synapses and memory in Aβ oligomer-treated rats.Journal of neuroinflammation · 2026Article
- Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.Cell communication and signaling : CCS · 2026Article
- Kaempferol Protects Against Amyloid β Overproduction and the Rise of Phospho-Tau 217 and Phospho-Tau 181 in the RatInternational journal of molecular sciences · 2026Article
- Herpes simplex virus-1 induces complement-mediated microglial phagocytosis of synapses in murine primary brain cultures and tissues.Cell communication and signaling : CCS · 2026Article
- Novel molecular mechanism driving neuroprotection after soluble epoxide hydrolase inhibition: Insights for Alzheimer's disease therapeutics.CNS neuroscience & therapeutics · 2024Article
- Proteomic association with age-dependent sex differences in Wisconsin Card Sorting Test performance in healthy Thai subjects.Scientific reports · 2023Article
- Complement C3 Enhances LPS-Elicited Neuroinflammation and Neurodegeneration Via the Mac1/NOX2 Pathway.Molecular neurobiology · 2023Article
- C/EBPβ Regulates TFAM Expression, Mitochondrial Function and Autophagy in Cellular Models of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Complement factor B is essential for the proper function of the peripheral auditory system.Frontiers in neurology · 2023Article
- The Complement System in the Central Nervous System: From Neurodevelopment to Neurodegeneration.Biomolecules · 2022Review
- DDX5 promotes oncogene C3 and FABP1 expressions and drives intestinal inflammation and tumorigenesis.Life science alliance · 2020Article
- Early Reactive A1 Astrocytes Induction by the Neurotoxin 3-Nitropropionic Acid in Rat Brain.International journal of molecular sciences · 2020Article
- Novel Approaches for the Treatment of Alzheimer's and Parkinson's Disease.International journal of molecular sciences · 2019Review
- Advances in the Potential Biomarkers of Epilepsy.Frontiers in neurology · 2019Review
- The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease.Frontiers in immunology · 2019Article
- High glucose-induced complement component 3 up-regulation via RAGE-p38MAPK-NF-κB signalling in astrocytes: In vivo and in vitro studies.Journal of cellular and molecular medicine · 2018Article
- CCAAT/Enhancer binding protein β silencing mitigates glial activation and neurodegeneration in a rat model of Parkinson's disease.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe 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.
methodsAdult male Wistar rats (8-12 weeks old) were used throughout the study. C/EBPβ
resultsIn 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.
conclusionsAltogether 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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