ArticleNeurochemical research2013
Reactive oxygen species from human astrocytes induced functional impairment and oxidative damage.
Article in Neurochemical research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 112 citations in OpenAlex.
- Review
- 7-ketocholesterol contributes to microglia-driven increases in astrocyte reactive oxygen species in a mouse model of Alzheimer's disease.Scientific reports · 2026Article
- Using combined ROC curves to improve the diagnostic usefulness of glutaminase, prostaglandins, and 8-isoprostane as biomarkers of autism spectrum disorders;Role in the Glu-GABA-Gln cycle.BMC neuroscience · 2026Article
- Article
- Microfluidic device to study spatial and temporal response of astrocyte networks in response to changes in the biochemical milieu.Microsystems & nanoengineering · 2026Article
- Characterizing insomnia and sleep quality in a cohort with tension type headache.Open medicine (Warsaw, Poland) · 2026Article
- Repurposing mitochondrial-targeting drugs for management of ICANS in CAR T-cell therapy: a novel steroid-sparing approach.Frontiers in pharmacology · 2026Article
- The Role of Interleukin-8 (IL-8) in Treatment-Resistant Depression: A Review of Mechanisms, Biomarker Potential, and Therapeutic Implications.International journal of molecular sciences · 2025Review
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Understanding monocyte-driven neuroinflammation in Alzheimer's disease using human cortical organoid microphysiological systems.Science advances · 2025Article
- Reactive Astrocytes in Glioma: Emerging Opportunities and Challenges.International journal of molecular sciences · 2025Review
- New perspectives on heterogeneity in astrocyte reactivity in neuroinflammation.Brain, behavior, & immunity - health · 2025Article
- Zinc signaling controls astrocyte-dependent synapse modulation via the PAF receptor pathway.Journal of neurochemistry · 2025Article
- Astrocyte-mediated inflammatory responses in traumatic brain injury: mechanisms and potential interventions.Frontiers in immunology · 2025Review
- The role of reactive oxygen species in the regulation of the blood-brain barrier.Tissue barriers · 2025Review
- Role of Oxidative Stress in the Occurrence and Development of Cognitive Dysfunction in Patients with Obstructive Sleep Apnea Syndrome.Molecular neurobiology · 2024Review
- The duality of amyloid-β: its role in normal and Alzheimer's disease states.Molecular brain · 2024Review
- Orchestrating Stress Responses in Multiple Sclerosis: A Role for Astrocytic IFNγ Signaling.International journal of molecular sciences · 2024Review
- Polar lipids modify Alzheimer's Disease pathology by reducing astrocyte pro-inflammatory signaling through platelet-activating factor receptor (PTAFR) modulation.Lipids in health and disease · 2024Article
- A novelFrontiers in cellular neuroscience · 2024Article
14 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) have been shown to be a contributor to aging and disease. ROS also serve as a trigger switch for signaling cascades leading to corresponding cellular and molecular events. In the central nervous system (CNS), microglial cells are likely the main source of ROS production. However, activated astrocytes also appear to be capable of generating ROS. In this study we investigated ROS production in human astrocytes stimulated with interleukin (IL)-1β and interferon (IFN)-γ and its potential harmful effects. Although IFN-γ alone had no effect, it potentiated IL-1β-induced ROS production in a time-dependent manner. One of the sources of ROS in IL-1β-activated astrocytes was from increased superoxide production in mitochondria accompanied by enhanced manganese superoxide dismutase and inhibited catalase expression. NADPH oxidase (NOX) may also contribute to ROS production as astrocytes express NOX isoforms. Glutamate uptake, which represents one of the most important methods of astrocytes to prevent excitotoxicity, was down-regulated in IL-1β-activated astrocytes, and was further suppressed in the presence of IFN-γ; IFN-γ itself exerted minimal effect. Elevated levels of 8-isoprostane in IL-1β ± IFN-γ-activated human astrocytes indicate downstream lipid peroxidation. Pretreatment with diphenyleneiodonium abolished the IL-1β ± IFN-γ-induced ROS production, restored glutamate uptake function and reduced 8-isoprostane to near control levels suggesting that ROS contributes to the dysfunction of activated astrocytes. These results support the notion that dampening activated human astrocytes to maintain the redox homeostasis is vital to preserve their neuroprotective potential in the CNS.
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