ArticleJournal of neurotrauma2018
A Single Primary Blast-Induced Traumatic Brain Injury in a Rodent Model Causes Cell-Type Dependent Increase in Nicotinamide Adenine Dinucleotide Phosphate Oxidase Isoforms in Vulnerable Brain Regions.
Article in Journal of neurotrauma, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 42 citations in OpenAlex.
- Sex and Genotype Affect Mouse Hippocampal Gene Expression in Response to Blast-Induced Traumatic Brain Injury.Molecular neurobiology · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Antisecretory Factor 16 (AF16): A Promising Avenue for the Treatment of Traumatic Brain Injury-An In Vitro Model Approach.Journal of molecular neuroscience : MN · 2024Article
- Phylogenetic conservation of the interdependent homeostatic relationship of sleep regulation and redox metabolism.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Review
- The effect of dietary omega-6 fatty acid enrichment in rodent models of military-relevant acute traumatic psychological stress and traumatic brain injury.Frontiers in microbiomes · 2024Article
- Twenty Years of Blast-Induced Neurotrauma: Current State of Knowledge.Neurotrauma reports · 2024Article
- Temporal Changes in Functional and Structural Neuronal Activities in Auditory System in Non-Severe Blast-Induced Tinnitus.Medicina (Kaunas, Lithuania) · 2023Article
- Ferroptosis: a critical player and potential therapeutic target in traumatic brain injury and spinal cord injury.Neural regeneration research · 2023Review
- Enhanced Targeted Delivery of Minocycline via Transferrin Conjugated Albumin Nanoparticle Improves Neuroprotection in a Blast Traumatic Brain Injury Model.Brain sciences · 2023Article
- Effect of minocycline and its nano-formulation on central auditory system in blast-induced hearing loss rat model.Journal of otology · 2023Article
- The Hidden Notes of Redox Balance in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2022Review
- Matrix Inversion and Subset Selection (MISS): A pipeline for mapping of diverse cell types across the murine brain.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Investigation of the direct and indirect mechanisms of primary blast insult to the brain.Scientific reports · 2021Article
- Oxidative stress contributes to cerebral metabolomic profile changes in animal model of blast-induced traumatic brain injury.Metabolomics : Official journal of the Metabolomic Society · 2020Article
- Glial Activation in the Thalamus Contributes to Vestibulomotor Deficits Following Blast-Induced Neurotrauma.Frontiers in neurology · 2020Article
- Microglia Receptors in Animal Models of Traumatic Brain Injury.Molecular neurobiology · 2019Review
- Synergistic Role of Oxidative Stress and Blood-Brain Barrier Permeability as Injury Mechanisms in the Acute Pathophysiology of Blast-induced Neurotrauma.Scientific reports · 2019Article
- Isoliquiritigenin Provides Protection and Attenuates Oxidative Stress-Induced Injuries via the Nrf2-ARE Signaling Pathway After Traumatic Brain Injury.Neurochemical research · 2018Article
- Oxidized phospholipid signaling in traumatic brain injury.Free radical biology & medicine · 2018Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Blast-induced traumatic brain injury (bTBI) is a leading cause of morbidity in soldiers on the battlefield and in training sites with long-term neurological and psychological pathologies. Previous studies from our laboratory demonstrated activation of oxidative stress pathways after blast injury, but their distribution among different brain regions and their impact on the pathogenesis of bTBI have not been explored. The present study examined the protein expression of two isoforms: nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 and 2 (NOX1, NOX2), corresponding superoxide production, a downstream event of NOX activation, and the extent of lipid peroxidation adducts of 4-hydroxynonenal (4HNE) to a range of proteins. Brain injury was evaluated 4 h after the shock-wave exposure, and immunofluorescence signal quantification was performed in different brain regions. Expression of NOX isoforms displayed a differential increase in various brain regions: in hippocampus and thalamus, there was the highest increase of NOX1, whereas in the frontal cortex, there was the highest increase of NOX2 expression. Cell-specific analysis of changes in NOX expression with respect to corresponding controls revealed that blast resulted in a higher increase of NOX1 and NOX 2 levels in neurons compared with astrocytes and microglia. Blast exposure also resulted in increased superoxide levels in different brain regions, and such changes were reflected in 4HNE protein adduct formation. Collectively, this study demonstrates that primary blast TBI induces upregulation of NADPH oxidase isoforms in different regions of the brain parenchyma and that neurons appear to be at higher risk for oxidative damage compared with other neural cells.
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