ArticlePloS one2013
Absence of TLR4 reduces neurovascular unit and secondary inflammatory process after traumatic brain injury in mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 2 of them syntheses that pooled it.
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Who cites it
75 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.
- Trauma-Related Guillain-Barré Syndrome: Systematic Review of an Emerging Concept.Frontiers in neurology · 2020Pooled it
- Evolution of mesenchymal stem cell therapies for traumatic brain injury: A decade of advances, mechanisms, and translational prospects.Cell transplantationPooled it
- Non-invasive Vagal Nerve Stimulation as a Potential Treatment for Repetitive Blast Trauma.bioRxiv : the preprint server for biology · 2026Article
- Neuronal toll-like receptor-4 regulation of matrix metalloproteinase-9 activity mediates dentate circuit dysfunction after traumatic brain injury.Journal of neuroinflammation · 2026Article
- The Neuroameliorative Effects of Enzymatically Modified Isoquercitrin and Sodium R-lipoate on the Rotenone rat Model of Parkinson's Disease.Neurochemical research · 2026Article
- Neuronal Toll-like Receptor-4 regulation of Matrix Metalloproteinase-9 Activity Mediates Dentate Circuit Dysfunction after Traumatic Brain Injury.bioRxiv : the preprint server for biology · 2026Article
- Neuroprotective mechanisms of nutraceutical berberine: Preclinical evidence and future perspectives.Advances in neurotoxicology · 2026Article
- Research Progress on Regulating Autophagy in Traditional Chinese Medicine for the Treatment of Traumatic Brain Injury.ACS omega · 2025Review
- TLR4 deficiency does not alter glaucomatous progression in a mouse model of chronic glaucoma.Scientific reports · 2025Article
- Administration of monophosphoryl lipid A shortly after traumatic brain injury blocks the following spatial and avoidance memory loss and neuroinflammation.Scientific reports · 2024Article
- Protective Effects of Plant-Derived Compounds Against Traumatic Brain Injury.Molecular neurobiology · 2024Review
- The contribution of the meningeal immune interface to neuroinflammation in traumatic brain injury.Journal of neuroinflammation · 2024Review
- Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression.International journal of molecular sciences · 2023Review
- Autophagy machinery plays an essential role in traumatic brain injury-induced apoptosis and its related behavioral abnormalities in mice: focus onFrontiers in physiology · 2023Article
- Galectin-3, a rising star in modulating microglia activation under conditions of neurodegeneration.Cell death & disease · 2022Review
- Neural stem cell therapy in conjunction with curcumin loaded in niosomal nanoparticles enhanced recovery from traumatic brain injury.Scientific reports · 2022Article
- Grape Seed Proanthocyanidins Exert a Neuroprotective Effect by Regulating Microglial M1/M2 Polarisation in Rats with Spinal Cord Injury.Mediators of inflammation · 2022Article
- Neuroinflammation Following Traumatic Brain Injury: Take It Seriously or Not.Frontiers in immunology · 2022Review
- Microglia-Dependent and Independent Brain Cytoprotective Effects of Mycophenolate Mofetil During Neuronal Damage.Frontiers in aging neuroscience · 2022Article
- Vitamin D Protects against Traumatic Brain Injury via Modulating TLR4/MyD88/NF-BioMed research international · 2022Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTraumatic brain injury (TBI) initiates a neuroinflammatory cascade that contributes to neuronal damage and behavioral impairment. Toll-like receptors (TLRs) are signaling receptors in the innate immune system, although emerging evidence indicates their role in brain injury. We have therefore investigated the role played by TLR4 signaling pathway in the development of mechanisms of secondary inflammatory process in traumatic brain injury (TBI) differ in mice that lack a functional TLR4 signaling pathway. METHODS/PRINCIPAL
findingsControlled cortical impact injury was performed on TLR4 knockout (KO) mice (C57BL/10ScNJ) and wild-type (WT) mice (C57BL/10ScNJ). TBI outcome was evaluated by determination of infarct volume and assessment of neurological scores. Brains were collected at 24 h after TBI. When compared to WT mice, TLR4 KO mice had lower infarct volumes and better outcomes in neurological and behavioral tests (evaluated by EBST and rotarod test). Mice that lacked TLR4 had minor expression of TBI-induced GFAP, Chymase, Tryptase, IL-1β, iNOS, PARP and Nitrotyrosine mediators implicated in brain damage. The translocation of expression of p-JNK, IκB-α and NF-κB pathway were also lower in brains from TLR4 KO mice. When compared to WT mice, resulted in significant augmentation of all the above described parameters. In addition, apoptosis levels in TLR4 KO mice had minor expression of Bax while on the contrary with Bcl-2. CONCLUSIONS/SIGNIFICANCE: Our results clearly demonstrated that absence of TLR4 reduces the development of neuroinflammation, tissues injury events associated with brain trauma and may play a neuroprotective role in TBI in mice.
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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.