ArticleArthritis and rheumatism2013
Acid-sensing ion channel 3 deficiency increases inflammation but decreases pain behavior in murine arthritis.
Article in Arthritis and rheumatism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 54 citations in OpenAlex.
- Concurrent Alterations in Selected mRNAs and miR-30 Family Members in Canine Osteoarthritic Joint Tissues.Biomedicines · 2026Article
- Ectopic Nociceptor Sprouting as a Key Peripheral Driver of Pain in Rheumatoid Arthritis.Current rheumatology reports · 2025Review
- A role for proprioceptors in sngception.Science advances · 2025Article
- Astrocyte activation in hindlimb somatosensory cortex contributes to electroacupuncture analgesia in acid-induced pain.Frontiers in neurology · 2024Article
- Role of proprioceptors in chronic musculoskeletal pain.Experimental physiology · 2024Review
- Experimental models to study osteoarthritis pain and develop therapeutics.Osteoarthritis and cartilage open · 2022Review
- Calcium-Permeable Channels Cooperation for Rheumatoid Arthritis: Therapeutic Opportunities.Biomolecules · 2022Review
- Article
- Neurodegenerative Disease: What Potential Therapeutic Role of Acid-Sensing Ion Channels?Frontiers in cellular neuroscience · 2021Review
- In silico screening of GMQ-like compounds reveals guanabenz and sephin1 as new allosteric modulators of acid-sensing ion channel 3.Biochemical pharmacology · 2020Article
- An overview of carbonic anhydrases and membrane channels of synoviocytes in inflamed joints.Journal of enzyme inhibition and medicinal chemistry · 2019Review
- Sensing acidosis: nociception or sngception?Journal of biomedical science · 2018Review
- TDAG8, TRPV1, and ASIC3 involved in establishing hyperalgesic priming in experimental rheumatoid arthritis.Scientific reports · 2017Article
- Novel Insights into Acid-Sensing Ion Channels: Implications for Degenerative Diseases.Aging and disease · 2016Review
- ASIC3 Is Required for Development of Fatigue-Induced Hyperalgesia.Molecular neurobiology · 2016Article
- Article
- ASICs Mediate Pain and Inflammation in Musculoskeletal Diseases.Physiology (Bethesda, Md.) · 2015Review
- Urinary N telopeptide levels in predicting the anti-nociceptive responses of zoledronic acid and paclitaxel in a rat model of bone metastases.Molecular medicine reports · 2015Article
- The dichotomized role for acid sensing ion channels in musculoskeletal pain and inflammation.Neuropharmacology · 2015Review
- Suppression of Peripheral Pain by Blockade of Voltage-Gated Calcium 2.2 Channels in Nociceptors Induces RANKL and Impairs Recovery From Inflammatory Arthritis in a Mouse Model.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveThrough its location on nociceptors, acid-sensing ion channel 3 (ASIC-3) is activated by decreases in pH and plays a significant role in musculoskeletal pain. We recently showed that decreases in pH activate ASIC-3 located on fibroblast-like synoviocytes (FLS), which are key cells in the inflammatory process. The purpose of this study was to test whether ASIC-3-deficient mice with arthritis have altered inflammation and pain relative to controls.
methodsCollagen antibody-induced arthritis (CAIA) was generated by injection of an anti-type II collagen antibody cocktail. Inflammation and pain parameters in ASIC-3(-/-) and ASIC-3(+/+) mice were assessed. Disease severity was assessed by determining clinical arthritis scores, measuring joint diameters, analyzing joint histology, and assessing synovial gene expression by quantitative polymerase chain reaction analysis. Cell death was assessed with a Live/Dead assay of FLS in response to decreases in pH. Pain behaviors in the mice were measured by examining withdrawal thresholds in the joints and paws and by measuring their physical activity levels.
resultsSurprisingly, ASIC-3(-/-) mice with CAIA demonstrated significantly increased joint inflammation, joint destruction, and expression of interleukin-6 (IL-6), matrix metalloproteinase 3 (MMP-3), and MMP-13 in joint tissue as compared to ASIC-3(+/+) mice. ASIC-3(+/+) FLS showed enhanced cell death when exposed to pH 6.0 in the presence of IL-1β, which was abolished in ASIC-3(-/-) FLS. Despite enhanced disease severity, ASIC-3(-/-) mice did not develop mechanical hypersensitivity of the paw and showed greater levels of physical activity.
conclusionOur findings are consistent with the hypothesis that ASIC-3 plays a protective role in the inflammatory arthritides by limiting inflammation through enhanced synoviocyte cell death, which reduces disease severity, and through the production of pain, which reduces joint use.
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Registered trials
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