ArticleNeurochemistry international2015
Antioxidant peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo.
Article in Neurochemistry international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- APOE genotype differentially modulates prion pathology in a mouse model.Acta neuropathologica communications · 2026Article
- APOE Genotype Differentially Modulates Prion Pathology in a Mouse Model.Research square · 2025Article
- Mitochondrial Gene Regulation and Pain Susceptibility: A Multi-Omics Causal Inference Study.International journal of molecular sciences · 2025Article
- Article
- Brosimine B and the biphasic dose-response: insights into hormesis and retinal neuroprotection.Frontiers in pharmacology · 2025Article
- Microglia-Astrocyte Crosstalk in Post-Stroke Neuroinflammation: Mechanisms and Therapeutic Strategies.Current neuropharmacology · 2025Review
- Neurological Biomarker Profiles in Royal Canadian Air Force (RCAF) Pilots and Aircrew.Brain sciences · 2024Article
- Chemical Hypoxic Preconditioning Improves Survival and Proliferation of Mesenchymal Stem Cells.Applied biochemistry and biotechnology · 2024Article
- Unveiling the Significance of Peroxiredoxin 6 in Central Nervous System Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- PRDX6-iPLA2 aggravates neuroinflammation after ischemic stroke via regulating astrocytes-induced M1 microglia.Cell communication and signaling : CCS · 2024Article
- Integrative analysis of multi-omics data for discovery of ferroptosis-related gene signature predicting immune activity in neuroblastoma.Frontiers in pharmacology · 2023Article
- Hydrogen peroxide-induced oxidative damage and protective role of peroxiredoxin 6 protein via EGFR/ERK signaling pathway in RPE cells.Frontiers in aging neuroscience · 2023Article
- PrPMolecular neurobiology · 2022Article
- Absence of Apolipoprotein E is associated with exacerbation of prion pathology and promotes microglial neurodegenerative phenotype.Acta neuropathologica communications · 2021Article
- The Roles of Peroxiredoxin 6 in Brain Diseases.Molecular neurobiology · 2021Review
- Enhanced contextual fear memory in peroxiredoxin 6 knockout mice is associated with hyperactivation of MAPK signaling pathway.Molecular brain · 2021Article
- Peroxiredoxin 6 mediates protective function of astrocytes in Aβ proteostasis.Molecular neurodegeneration · 2020Article
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- RNA editing alterations define manifestation of prion diseases.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Protein misfolding, mitochondrial dysfunction and oxidative stress are common pathomechanisms that underlie neurodegenerative diseases. In prion disease, central to these processes is the post-translational transformation of cellular prion protein (PrP(c)) to the aberrant conformationally altered isoform; PrP(Sc). This can trigger oxidative reactions and impair mitochondrial function by increasing levels of peroxynitrite, causing damage through formation of hydroxyl radicals or via nitration of tyrosine residues on proteins. The 6 member Peroxiredoxin (Prdx) family of redox proteins are thought to be critical protectors against oxidative stress via reduction of H2O2, hydroperoxides and peroxynitrite. In our in vitro studies cellular metabolism of SK-N-SH human neuroblastoma cells was significantly decreased in the presence of H2O2 (oxidative stressor) or CoCl2 (cellular hypoxia), but was rescued by treatment with exogenous Prdx6, suggesting that its protective action is in part mediated through a direct action. We also show that CoCl2-induced apoptosis was significantly decreased by treatment with exogenous Prdx6. We proposed a redox regulator role for Prdx6 in regulating and maintaining cellular homeostasis via its ability to control ROS levels that could otherwise accelerate the emergence of prion-related neuropathology. To confirm this, we established prion disease in mice with and without astrocyte-specific antioxidant protein Prdx6, and demonstrated that expression of Prdx6 protein in Prdx6 Tg ME7-animals reduced severity of the behavioural deficit, decreased neuropathology and increased survival time compared to Prdx6 KO ME7-animals. We conclude that antioxidant Prdx6 attenuates prion-related neuropathology, and propose that augmentation of endogenous Prdx6 protein represents an attractive adjunct therapeutic approach for neurodegenerative diseases.
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