ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Exacerbation of damage and altered NF-kappaB activation in mice lacking tumor necrosis factor receptors after traumatic brain injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 270 citations in OpenAlex.
- Cytokine Responses in Severe Traumatic Brain Injury: Where There Is Smoke, Is There Fire?Neurocritical care · 2019Pooled it
- Repurposing Leucovorin for Mild Traumatic Brain Injury: Evidence from Biochemical and Behavioral Outcomes in Rats.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Genetic variation in innate immune gene expression influences mortality after traumatic brain injury in Drosophila.G3 (Bethesda, Md.) · 2026Article
- Antiretroviral drug therapy does not reduce neuroinflammation in an HIV-1 infection brain organoid model.Journal of neuroinflammation · 2025Article
- Primed inflammatory response by fibroblast subset is necessary for proper oral and cutaneous wound healing.Molecular oral microbiology · 2024Article
- The role of mitochondrial uncoupling in the regulation of mitostasis after traumatic brain injury.Neurochemistry international · 2024Article
- Edaravone Confers Neuroprotective, Anti-inflammatory, and Antioxidant Effects on the Fetal Brain of a Placental-ischemia Mouse Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Article
- Article
- Characterizing Sex Differences in Mitochondrial Dysfunction After Severe Traumatic Brain Injury in Mice.Neurotrauma reports · 2023Article
- The role of diphenhydramine HCl on tumor necrosis factor-α levels in wistar rats with traumatic brain injury: An in vivo study.Annals of medicine and surgery (2012) · 2022Article
- Acute minocycline administration reduces brain injury and improves long-term functional outcomes after delayed hypoxemia following traumatic brain injury.Acta neuropathologica communications · 2022Article
- Neurological Symptoms and Their Associations With Inflammatory Biomarkers in the Chronic Phase Following Traumatic Brain Injuries.Frontiers in psychiatry · 2022Article
- Traumatic Brain Injury: Mechanistic Insight on Pathophysiology and Potential Therapeutic Targets.Journal of molecular neuroscience : MN · 2021Review
- 3,6'-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury.International journal of molecular sciences · 2021Article
- Molecular and cellular pathways contributing to brain aging.Behavioral and brain functions : BBF · 2021Review
- Article
- Gut microbial dysbiosis after traumatic brain injury modulates the immune response and impairs neurogenesis.Acta neuropathologica communications · 2021Article
- Survival Following Traumatic Brain Injury inGenetics · 2020Article
- Down-regulation of ROCK2 alleviates ethanol-induced cerebral nerve injury partly by the suppression of the NF-κB signaling pathway.Bioengineered · 2020Article
- Article
45 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Tumor necrosis factor alpha (TNFalpha) is widely expressed in both neurons and glia and has been shown to be upregulated after traumatic brain injury (TBI). TNFalpha receptor activation results in activation of the transcription factor nuclear factor kappaB (NF-kappaB), which may serve an antiapoptotic role via the induction of target genes manganese superoxide dismutase (MnSOD) and/or calbindin. In the present study, we used a controlled cortical impact model of TBI with pertinent lines of transgenic mice to combine both morphological characterization and molecular analysis to elucidate the role of TNFalpha after TBI. Measurements of both the lesion volume and the blood-brain barrier breach indicated exacerbations in mice rendered genetically deficient in both the p55 and p75 TNFalpha receptors (TNFR-KO) compared with wild-type animals. Additionally, animals genetically altered to overexpress MnSOD showed a significant decrease in lesion volume compared with that of control littermates, whereas no alterations were observed in mice lacking the calcium-binding protein calbindin D28k. Analysis of NF-kappaB activation and relative levels of MnSOD revealed delayed responses in the injured cortex of TNFR-KO animals compared with wild-type animals, implying that endogenous TNFalpha may be neuroprotective after TBI.
Indexed as
Identifiers
10414954PMC6782813W1603434131What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.