ArticleJournal of neurochemistry2010
The cyclooxygenase site, but not the peroxidase site of cyclooxygenase-2 is required for neurotoxicity in hypoxic and ischemic injury.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
12 citing papers in PubMed, 27 citations in OpenAlex.
- Targeting Lipid Peroxidation for Cancer Treatment.Molecules (Basel, Switzerland) · 2020Review
- Cyclosporine A binding to COX-2 reveals a novel signaling pathway that activates the IRE1α unfolded protein response sensor.Scientific reports · 2018Article
- Impact of novel N-aryl piperamide NO donors on NF-κB translocation in neuroinflammation: rational drug-designing synthesis and biological evaluation.Innate immunity · 2018Article
- COX2 is involved in hypoxia-induced TNF-α expression in osteoblast.Scientific reports · 2015Article
- Protein disulfide isomerase as a novel target for cyclopentenone prostaglandins: implications for hypoxic ischemic injury.The FEBS journal · 2015Article
- Increased cytochrome c in rat cerebrospinal fluid after cardiac arrest and its effects on hypoxic neuronal survival.Resuscitation · 2012Article
- A high-throughput screening assay of ascorbate in brain samples.Journal of neuroscience methods · 2011Article
- Superoxide generation catalyzed by the ozone-inducible plant peptides analogous to prion octarepeat motif.Plant signaling & behavior · 2011Article
- Modification of ubiquitin-C-terminal hydrolase-L1 by cyclopentenone prostaglandins exacerbates hypoxic injury.Neurobiology of disease · 2011Article
- Fluorescent monitoring of copper-occupancy in His-ended catalytic oligo-peptides.Communicative & integrative biologyArticle
- Production and removal of superoxide anion radical by artificial metalloenzymes and redox-active metals.Communicative & integrative biologyReview
- COX-2 in the neurodegenerative process of Parkinson's disease.BioFactors (Oxford, England)Review
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Cyclooxygenase-2 (COX-2) activity has been implicated in the pathogenesis of ischemic injury, but the exact mechanisms responsible for its toxicity remain unclear. Infection of primary neurons with an adenovirus expressing wild type (WT) COX-2 increased the susceptibility of neurons to hypoxia. Infection with an adenoviral vector expressing COX-2 with a mutation at the cyclooxygenase site did not increase susceptibility to hypoxia, whereas over-expression of COX-2 with a mutation in the peroxidase site produced similar susceptibility to hypoxia as WT COX-2. Primary neuronal cultures obtained from transgenic mice bearing a mutation in the COX-2 cylooxygenase site were protected from hypoxia. Mice with a mutation in the cyclooxygenase site had smaller infarctions 24 h after 70 min of middle cerebral artery occlusion than WT control mice. COX-2 activity had no effect on the formation of protein carbonyls. Ascorbate radicals were detected by electron paramagnetic resonance as a product of recombinant COX-2 activity and were blocked by COX-2 inhibitors. Similarly, formation of ascorbate radicals was inhibited in the presence of COX-2 inhibitors and in homogenates obtained from COX-2 null mice. Taken together, these results indicate that the cyclooxygenase activity of COX-2 is necessary to exacerbate neuronal hypoxia/ischemia injury rather than the peroxidase activity of the enzyme.
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Registered trials
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