ArticleJournal of neuroinflammation2013
Cellular and temporal expression of NADPH oxidase (NOX) isotypes after brain injury.
Article in Journal of neuroinflammation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 153 citations in OpenAlex.
- Tracking CNS and systemic sources of oxidative stress during the course of chronic neuroinflammation.Acta neuropathologica · 2015Trial
- Dynamic metabolic programming of monocyte-derived cells defines immunity in CNS disease.Brain : a journal of neurology · 2026Review
- Reprogramming the oxidative microenvironment: Antioxidant nanoplatforms for central nervous system repair.Materials today. Bio · 2026Review
- Fibrinogen as a Driver of Oxidative Stress and Apoptosis in the Fetal Brain After Maternal Influenza.Research square · 2026Article
- Tibolone Administration Is Associated with Enhanced Motor Recovery and Decreased Cell-Specific NOX2 and NOX4 Immunoreactivity in a Rat Model of Traumatic Spinal Cord Injury.Brain sciences · 2026Article
- RvD1/FPR2 attenuates cerebral ischemic injury through inhibiting inflammation and oxidative stress.Scientific reports · 2026Article
- Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026Review
- Reprogramming brain-resident macrophages: from disease drivers to therapeutic allies in neurological disorders.Frontiers in cellular neuroscience · 2026Review
- Neuroprotective effects of cobalt oxide nanoparticles through mitigating oxidative stress and reactive glial responses in traumatic brain injury.Materials today. Bio · 2025Article
- Human Neural Progenitor Cell-Derived Exosomes Deliver miR- 100 - 5p Targeting NOX4 mRNA to Alleviate Oxidative Stress in Acute Ischemia Injury.Molecular neurobiology · 2025Article
- Autophagy hub-protein p62 orchestrates oxidative, endoplasmic reticulum stress, and inflammatory responses post-ischemia, exacerbating stroke outcome.Redox biology · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Effects of iron accumulation and its chelation on oxidative stress in intracortical implants.Acta biomaterialia · 2025Article
- Mitochondrial-targeted therapies in traumatic brain injury: From bench to bedside.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- α-Pyrrolidinooctanophenone facilitates activation of human microglial cells via ROS/STAT3-dependent pathway.Forensic toxicology · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- NOX proteins and ROS generation: role in invadopodia formation and cancer cell invasion.Biological research · 2024Review
- Inflammation and DNA methylation in Alzheimer's disease: mechanisms of epigenetic remodelling by immune cell oxidants in the ageing brain.Redox report : communications in free radical research · 2024Review
- Pediatric Acute-Onset Neuropsychiatric Syndrome (PANS) and Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS): Immunological Features Underpinning Controversial Entities.Children (Basel, Switzerland) · 2024Review
- β-Hydroxybutyrate Improves the Redox Status, Cytokine Production and Phagocytic Potency of Glucose-Deprived HMC3 Human Microglia-like Cells.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
43 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBrain injury results in an increase in the activity of the reactive oxygen species generating NADPH oxidase (NOX) enzymes. Preliminary studies have shown that NOX2, NOX3, and NOX4 are the most prominently expressed NOX isotypes in the brain. However, the cellular and temporal expression profile of these isotypes in the injured and non-injured brain is currently unclear.
methodsDouble immunofluorescence for NOX isotypes and brain cell types was performed at acute (24 hours), sub-acute (7 days), and chronic (28 days) time points after controlled cortical impact-induced brain injury or sham-injury in rats.
resultsNOX2, NOX3, and NOX4 isotypes were found to be expressed in neurons, astrocytes, and microglia, and this expression was dependent on both cellular source and post-injury time. NOX4 was found in all cell types assessed, while NOX3 was positively identified in neurons only, and NOX2 was identified in microglia and neurons. NOX2 was the most responsive to injury, increasing primarily in microglia in response to injury. Quantitation of this isotype showed a significant increase in NOX2 expression at 24 hours, with reduced expression at 7 days and 28 days post-injury, although expression remained above sham levels at later time points. Cellular confirmation using purified primary or cell line culture demonstrated similar patterns in microglia, astrocytes, and neurons. Further, inhibition of NOX, and more specifically NOX2, reduced pro-inflammatory activity in microglia, demonstrating that NOX is not only up-regulated after stimulation, but may also play a significant role in post-injury neuroinflammation.
conclusionsThis study illustrates the expression profiles of NOX isotypes in the brain after injury, and demonstrates that NOX2, and to a lesser extent, NOX4, may be responsible for the majority of oxidative stress observed acutely after traumatic brain injury. These data may provide insight into the design of future therapeutic approaches.
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