ArticleThe Journal of clinical investigation2009
COX2 in CNS neural cells mediates mechanical inflammatory pain hypersensitivity in mice.
Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
59 citing papers in PubMed, 136 citations in OpenAlex.
- Betanin fromBiomedicines · 2026Article
- Drugs in Development to Manage Acute Pain.Drugs · 2025Review
- Ferroptosis in pain: evidence, challenges, and opportunities.Frontiers in immunology · 2025Review
- PTGS2 Is Involved in Osteonecrosis of the Femoral Head and Bone Marrow Edema.International journal of genomics · 2025Article
- Assessing the COX-2/PGE2 Ratio and Anti-Nucleosome Autoantibodies as Biomarkers of Autism Spectrum Disorders: Using Combined ROC Curves to Improve Diagnostic Values.Current issues in molecular biology · 2024Article
- Lipocalin-2 Secreted by the Liver Regulates Neuronal Cell Function Through AKT-Dependent Signaling in Hepatic Encephalopathy Mouse Model.Clinical nutrition research · 2023Article
- Inhibition of DAGLβ as a therapeutic target for pain in sickle cell disease.Haematologica · 2023Article
- The Role of COX-2 and PGE2 in the Regulation of Immunomodulation and Other Functions of Mesenchymal Stromal Cells.Biomedicines · 2023Review
- Axon Guidance Molecules and Pain.Cells · 2022Review
- Organic anion transporter 1 is an HDAC4-regulated mediator of nociceptive hypersensitivity in mice.Nature communications · 2022Article
- Organic anion transporter 1 is an HDAC4-regulated mediator of nociceptive hypersensitivity in mice.Nature communications · 2022Article
- Can Endometriosis-Related Oxidative Stress Pave the Way for New Treatment Targets?International journal of molecular sciences · 2021Review
- Impact of Non-steroidal Anti-inflammatory Drug Administration for 12 Months on Renal Function.Frontiers in pain research (Lausanne, Switzerland) · 2021Article
- Nuclear Factor κB-COX2 Pathway Activation in Non-myelinating Schwann Cells Is Necessary for the Maintenance of Neuropathic PainFrontiers in cellular neuroscience · 2021Article
- Identification of a Pharmacological Biomarker for the Bioassay-Based Quality Control of a Thirteen-Component TCM Formula (Lianhua Qingwen) Used in Treating Influenza A Virus (H1N1) Infection.Frontiers in pharmacology · 2020Article
- The Molecular Signatures of Acute-immobilization-induced Antinociception and Chronic-immobilization-induced Antinociceptive Tolerance.Experimental neurobiology · 2019Article
- Macrophage-derived insulin-like growth factor-1 is a key neurotrophic and nerve-sensitizing factor in pain associated with endometriosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Characterization of gene expression in naturally occurring feline degenerative joint disease-associated pain.Veterinary journal (London, England : 1997) · 2019Article
- Cyclooxygenase-2 in Endometriosis.International journal of biological sciences · 2019Review
- Neurons and Microglia; A Sickly-Sweet Duo in Diabetic Pain Neuropathy.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
A cardinal feature of peripheral inflammation is pain. The most common way of managing inflammatory pain is to use nonsteroidal antiinflammatory agents (NSAIDs) that reduce prostanoid production, for example, selective inhibitors of COX2. Prostaglandins produced after induction of COX2 in immune cells in inflamed tissue contribute both to the inflammation itself and to pain hypersensitivity, acting on peripheral terminals of nociceptors. COX2 is also induced after peripheral inflammation in neurons in the CNS, where it aids in developing a central component of inflammatory pain hypersensitivity by increasing neuronal excitation and reducing inhibition. We engineered mice with conditional deletion of Cox2 in neurons and glial cells to determine the relative contribution of peripheral and central COX2 to inflammatory pain hypersensitivity. In these mice, basal nociceptive pain was unchanged, as was the extent of peripheral inflammation, inflammatory thermal pain hypersensitivity, and fever induced by lipopolysaccharide. By contrast, peripheral inflammation-induced COX2 expression in the spinal cord was reduced, and mechanical hypersensitivity after both peripheral soft tissue and periarticular inflammation was abolished. Mechanical pain is a major symptom of most inflammatory conditions, such as postoperative pain and arthritis, and induction of COX2 in neural cells in the CNS seems to contribute to this.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.