ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
The p38α MAPK regulates microglial responsiveness to diffuse traumatic brain injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 127 citations in OpenAlex.
- Photobiomodulation for the treatment of neuroinflammation: A systematic review of controlled laboratory animal studies.Frontiers in neuroscience · 2022Pooled it
- Inhibition of p38 MAPK after repetitive mTBI ameliorates immune signaling and functional deficits.Acta neuropathologica communications · 2026Article
- Revisiting the critical roles of reactive microglia in traumatic brain injury.International journal of surgery (London, England) · 2025Review
- p38α Mitogen-Activated Protein Kinase-An Emerging Drug Target for the Treatment of Alzheimer's Disease.Molecules (Basel, Switzerland) · 2024Review
- Role of mitochondrial dysfunction in acute traumatic brain injury: Evidence from bioinformatics analysis.Heliyon · 2024Article
- Pathophysiology of acute lung injury in patients with acute brain injury: the triple-hit hypothesis.Critical care (London, England) · 2024Review
- Cellular signaling pathways in the nervous system activated by various mechanical and electromagnetic stimuli.Frontiers in molecular neuroscience · 2024Review
- Reactive gliosis in traumatic brain injury: a comprehensive review.Frontiers in cellular neuroscience · 2024Review
- Old Age Exacerbates White Matter Neuroinflammation and Cognitive Deficits Following Closed-Head Injury, Particularly in Female Mice.Neurotrauma reports · 2024Article
- Tolerized Microglia Protect Neurons Against Endotoxin-Induced TNF-α Production via an LBP-Dependent Intracellular p38 MAPK Signaling Pathway.Inflammation · 2023Article
- Intranasally administered human MSC-derived extracellular vesicles inhibit NLRP3-p38/MAPK signaling after TBI and prevent chronic brain dysfunction.Brain, behavior, and immunity · 2023Article
- Novel image analysis tool for rapid screening of cell morphology in preclinical animal models of disease.Heliyon · 2023Article
- Regulation of microglial responses after pediatric traumatic brain injury: exploring the role of SHIP-1.Frontiers in neuroscience · 2023Article
- A single intranasal dose of human mesenchymal stem cell-derived extracellular vesicles after traumatic brain injury eases neurogenesis decline, synapse loss, and BDNF-ERK-CREB signaling.Frontiers in molecular neuroscience · 2023Article
- DICAM in the Extracellular Vesicles from Astrocytes Attenuates Microglia Activation and Neuroinflammation.Cells · 2022Article
- A Focal Impact Model of Traumatic Brain Injury inInternational journal of molecular sciences · 2022Article
- Chronic Cortical Inflammation, Cognitive Impairment, and Immune Reactivity Associated with Diffuse Brain Injury Are Ameliorated by Forced Turnover of Microglia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Neuronal chemokine-like-factor 1 (CKLF1) up-regulation promotes M1 polarization of microglia in rat brain after stroke.Acta pharmacologica Sinica · 2022Article
- Potential benefit of olive leaf extract in cervical spondylotic myelopathy model.Annals of medicine and surgery (2012) · 2022Article
- Naltrexone is neuroprotective against traumatic brain injury in mu opioid receptor knockout mice.CNS neuroscience & therapeutics · 2021Article
25 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Neuropathology after traumatic brain injury (TBI) is the result of both the immediate impact injury and secondary injury mechanisms. Unresolved post-traumatic glial activation is a secondary injury mechanism that contributes to a chronic state of neuroinflammation in both animal models of TBI and human head injury patients. We recently demonstrated, using in vitro models, that p38α MAPK signaling in microglia is a key event in promoting cytokine production in response to diverse disease-relevant stressors and subsequent inflammatory neuronal dysfunction. From these findings, we hypothesized that the p38α signaling pathway in microglia could be contributing to the secondary neuropathologic sequelae after a diffuse TBI. Mice where microglia were p38α-deficient (p38α KO) were protected against TBI-induced motor deficits and synaptic protein loss. In wild-type (WT) mice, diffuse TBI produced microglia morphological activation that lasted for at least 7 d; however, p38α KO mice failed to activate this response. Unexpectedly, we found that the peak of the early, acute phase cytokine and chemokine levels was increased in injured p38α KO mice compared with injured WT mice. The increased cytokine levels in the p38α KO mice could not be accounted for by more infiltration of macrophages or neutrophils, or increased astrogliosis. By 7 d after injury, the cytokine and chemokine levels remained elevated in injured WT mice but not in p38α KO mice. Together, these data suggest that p38α balances the inflammatory response by acutely attenuating the early proinflammatory cytokine surge while perpetuating the chronic microglia activation after TBI.
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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.