ArticlePLoS pathogens2014
The role of the NADPH oxidase NOX2 in prion pathogenesis.
Article in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 59 citations in OpenAlex.
- Apocynin, an NADPH Oxidase Enzyme Inhibitor, Prevents Amebic Liver Abscess in Hamster.Biomedicines · 2023Article
- Current Understanding of Long-Term Cognitive Impairment After Sepsis.Frontiers in immunology · 2022Review
- Review
- Reduced SOD2 expression does not influence prion disease course or pathology in mice.PloS one · 2021Article
- Genome-wide transcriptomics identifies an early preclinical signature of prion infection.PLoS pathogens · 2020Article
- Mitochondrial respiratory chain deficiency correlates with the severity of neuropathology in sporadic Creutzfeldt-Jakob disease.Acta neuropathologica communications · 2020Article
- Region-specific glial homeostatic signature in prion diseases is replaced by a uniform neuroinflammation signature, common for brain regions and prion strains with different cell tropism.Neurobiology of disease · 2020Article
- Modeling α-Synucleinopathy in Organotypic Brain Slice Culture with Preformed α-Synuclein Amyloid Fibrils.Journal of Parkinson's disease · 2020Article
- The role of NOX inhibitors in neurodegenerative diseases.IBRO reports · 2019Review
- Early Celastrol Administration Prevents Ketamine-Induced Psychotic-Like Behavioral Dysfunctions, Oxidative Stress and IL-10 Reduction in The Cerebellum of Adult Mice.Molecules (Basel, Switzerland) · 2019Article
- SARM1 deficiency up-regulates XAF1, promotes neuronal apoptosis, and accelerates prion disease.The Journal of experimental medicine · 2019Article
- Epigenetic Control of the Notch and Eph Signaling Pathways by the Prion Protein: Implications for Prion Diseases.Molecular neurobiology · 2019Article
- Prionoid Proteins in the Pathogenesis of Neurodegenerative Diseases.Frontiers in molecular neuroscience · 2019Review
- Region-Specific Response of Astrocytes to Prion Infection.Frontiers in neuroscience · 2019Article
- Guidelines for the Detection of NADPH Oxidases by Immunoblot and RT-qPCR.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Microglia in neurodegeneration.Nature neuroscience · 2018Review
- Prion protein cleavage fragments regulate adult neural stem cell quiescence through redox modulation of mitochondrial fission and SOD2 expression.Cellular and molecular life sciences : CMLS · 2018Article
- Inflammatory response of microglia to prions is controlled by sialylation of PrPScientific reports · 2018Article
- Inhibition of NADPH oxidase 2 induces apoptosis in osteosarcoma: The role of reactive oxygen species in cell proliferation.Oncology letters · 2018Article
- Inhibition of group-I metabotropic glutamate receptors protects against prion toxicity.PLoS pathogens · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prion infections cause neurodegeneration, which often goes along with oxidative stress. However, the cellular source of reactive oxygen species (ROS) and their pathogenetic significance are unclear. Here we analyzed the contribution of NOX2, a prominent NADPH oxidase, to prion diseases. We found that NOX2 is markedly upregulated in microglia within affected brain regions of patients with Creutzfeldt-Jakob disease (CJD). Similarly, NOX2 expression was upregulated in prion-inoculated mouse brains and in murine cerebellar organotypic cultured slices (COCS). We then removed microglia from COCS using a ganciclovir-dependent lineage ablation strategy. NOX2 became undetectable in ganciclovir-treated COCS, confirming its microglial origin. Upon challenge with prions, NOX2-deficient mice showed delayed onset of motor deficits and a modest, but significant prolongation of survival. Dihydroethidium assays demonstrated a conspicuous ROS burst at the terminal stage of disease in wild-type mice, but not in NOX2-ablated mice. Interestingly, the improved motor performance in NOX2 deficient mice was already measurable at earlier stages of the disease, between 13 and 16 weeks post-inoculation. We conclude that NOX2 is a major source of ROS in prion diseases and can affect prion pathogenesis.
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