ArticleJournal of neuroinflammation2016
Cell cycle inhibition reduces inflammatory responses, neuronal loss, and cognitive deficits induced by hypobaria exposure following traumatic brain injury.
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 23 papers, 2 of them syntheses that pooled it.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 47 citations in OpenAlex.
- From Mechanism to Therapy: Isoliquiritigenin as a Novel Anti-Inflammatory Agent for Inflammatory Disease ManagementEndocrine, metabolic & immune disorders drug targets · 2026Pooled it
- A comprehensive transcriptional reference for severity and progression in spinal cord injury reveals novel translational biomarker genes.Journal of translational medicine · 2025Pooled it
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- Inflammatory Factors Derived From Metabolic Dysfunction-Alcoholic Fatty Liver Disease: Inducers of Anxiety and Spatial Memory Impairment.Mediators of inflammation · 2026Article
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Integrated Transcriptomics and Metabolomics Reveal Changes in Cell Homeostasis and Energy Metabolism inInternational journal of molecular sciences · 2024Article
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- FDA-Approved Kinase Inhibitors in Preclinical and Clinical Trials for Neurological Disorders.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Nurr1 Modulation Mediates Neuroprotective Effects of Statins.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Decoding competitive endogenous RNA regulatory network in postoperative cognitive dysfunction.Frontiers in neuroscience · 2022Article
- Preclinical Western Blot in the Era of Digital Transformation and Reproducible Research, an Eastern Perspective.Interdisciplinary sciences, computational life sciences · 2021Article
- Functions and Mechanisms of the Voltage-Gated Proton Channel Hv1 in Brain and Spinal Cord Injury.Frontiers in cellular neuroscience · 2021Review
- Recovery of Depleted miR-146a in ALS Cortical Astrocytes Reverts Cell Aberrancies and Prevents Paracrine Pathogenicity on Microglia and Motor Neurons.Frontiers in cell and developmental biology · 2021Article
- Core cell cycle machinery is crucially involved in both life and death of post-mitotic neurons.Cellular and molecular life sciences : CMLS · 2020Review
- CDK4 and CDK5 Inhibition Have Comparable Mild Hypothermia Effects in Preventing Drp1-Dependent Mitochondrial Fission and Neuron Death Induced by MPPMolecular neurobiology · 2020Article
- Dementia, Depression, and Associated Brain Inflammatory Mechanisms after Spinal Cord Injury.Cells · 2020Review
- Neuroinflammation trajectories precede cognitive impairment after experimental meningitis-evidence from an in vivo PET study.Journal of neuroinflammation · 2020Article
- Aberrant cell cycle induction is pivotal for mitochondrial biogenesis after traumatic brain injury.Neural regeneration research · 2019Article
- Incretin Mimetics as Rational Candidates for the Treatment of Traumatic Brain Injury.ACS pharmacology & translational science · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
backgroundTraumatic brain injury (TBI) patients in military settings can be exposed to prolonged periods of hypobaria (HB) during aeromedical evacuation. Hypobaric exposure, even with supplemental oxygen to prevent hypoxia, worsens outcome after experimental TBI, in part by increasing neuroinflammation. Cell cycle activation (CCA) after TBI has been implicated as a mechanism contributing to both post-traumatic cell death and neuroinflammation. Here, we examined whether hypobaric exposure in rats subjected to TBI increases CCA and microglial activation in the brain, as compared to TBI alone, and to evaluate the ability of a cyclin-dependent kinase (CDK) inhibitor (CR8) to reduce such changes and improve behavioral outcomes.
methodsAdult male Sprague Dawley rats were subjected to fluid percussion-induced injury, and HB exposure was performed at 6 h after TBI. Western blot and immunohistochemistry (IHC) were used to assess cell cycle-related protein expression and inflammation at 1 and 30 days after injury. CR8 was administered intraperitoneally at 3 h post-injury; chronic functional recovery and histological changes were assessed.
resultsPost-traumatic hypobaric exposure increased upregulation of cell cycle-related proteins (cyclin D1, proliferating cell nuclear antigen, and CDK4) and microglial/macrophage activation in the ipsilateral cortex at day 1 post-injury as compared to TBI alone. Increased immunoreactivity of cell cycle proteins, as well as numbers of Iba-1
conclusionsHB exposure following TBI increases CCA, neuroinflammation, and associated neuronal cell loss. These changes and post-traumatic cognitive deficits are reduced by CDK inhibition; such drugs may therefore serve to protect TBI patients requiring aeromedical evacuation.
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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.