ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2015
S100B inhibition reduces behavioral and pathologic changes in experimental traumatic brain injury.
Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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The trial behind it
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.
- Fluid Biomarkers of Neuro-Glial Injury in Human Status Epilepticus: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Repurposing of high-dose N-acetylcysteine as anti-inflammatory, antioxidant and neuroprotective agent in moderate to severe traumatic brain injury patients: a randomized controlled trial.Inflammopharmacology · 2025Trial
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- Gastrodin inhibits reactive astrocyte-mediated inflammation in hypoxic-ischemic brain damage through S100B/RAGE-Smad3 signaling.Acta biochimica et biophysica Sinica · 2025Article
- Commentary on Boswellia and Ginger for Memory Dysfunction in Mild TBI.Bulletin of emergency and trauma · 2025Article
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Past, present, and future of cell replacement therapy for parkinson's disease: a novel emphasis on host immune responses.Cell research · 2024Review
- The S100B Protein: A Multifaceted Pathogenic Factor More Than a Biomarker.International journal of molecular sciences · 2023Review
- S100B, Actor and Biomarker of Mild Traumatic Brain Injury.International journal of molecular sciences · 2023Review
- Partial Ablation of Astrocytes Exacerbates Cerebral Infiltration of Monocytes and Neuronal Loss After Brain Stab Injury in Mice.Cellular and molecular neurobiology · 2023Article
- The role and potential therapeutic targets of astrocytes in central nervous system demyelinating diseases.Frontiers in cellular neuroscience · 2023Review
- The role of S100B/RAGE-enhanced ADAM17 activation in endothelial glycocalyx shedding after traumatic brain injury.Journal of neuroinflammation · 2022Article
- Pathophysiological Responses and Roles of Astrocytes in Traumatic Brain Injury.International journal of molecular sciences · 2021Review
- Reactive Astrocytes in Central Nervous System Injury: Subgroup and Potential Therapy.Frontiers in cellular neuroscience · 2021Review
- Research Progress on the Role of Inflammatory Mechanisms in the Development of Postoperative Cognitive Dysfunction.BioMed research international · 2021Review
- Microglia Receptors in Animal Models of Traumatic Brain Injury.Molecular neurobiology · 2019Review
- Characterization of Biaxial Stretch as an In Vitro Model of Traumatic Brain Injury to the Blood-Brain Barrier.Molecular neurobiology · 2018Article
- White matter damage after traumatic brain injury: A role for damage associated molecular patterns.Biochimica et biophysica acta. Molecular basis of disease · 2017Review
- Sterile Neuroinflammation and Strategies for Therapeutic Intervention.International journal of inflammation · 2017Review
- Microglial activation induced by the alarmin S100B is regulated by poly(ADP-ribose) polymerase-1.Glia · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Neuroinflammation following traumatic brain injury (TBI) is increasingly recognized to contribute to chronic tissue loss and neurologic dysfunction. Circulating levels of S100B increase after TBI and have been used as a biomarker. S100B is produced by activated astrocytes and can promote microglial activation; signaling by S100B through interaction with the multiligand advanced glycation end product-specific receptor (AGER) has been implicated in brain injury and microglial activation during chronic neurodegeneration. We examined the effects of S100B inhibition in a controlled cortical impact model, using S100B knockout mice or administration of neutralizing S100B antibody. Both interventions significantly reduced TBI-induced lesion volume, improved retention memory function, and attenuated microglial activation. The neutralizing antibody also significantly reduced sensorimotor deficits and improved neuronal survival in the cortex. However, S100B did not alter microglial activation in BV2 cells or primary microglial cultures stimulated by lipopolysaccharide or interferon gamma. Further, proximity ligation assays did not support direct interaction in the brain between S100B and AGER following TBI. Future studies are needed to elucidate specific pathways underlying S100B-mediated neuroinflammatory actions after TBI. Our results strongly implicate S100B in TBI-induced neuroinflammation, cell loss, and neurologic dysfunction, thereby indicating that it is a potential therapeutic target for TBI.
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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.