ArticleArthritis research & therapy2013
The progressive ankylosis gene product ANK regulates extracellular ATP levels in primary articular chondrocytes.
Article in Arthritis research & therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 42 citations in OpenAlex.
- A novel murine model of early calcium pyrophosphate deposition disease based on the TNFRSF11B mutation mimics features of the human disease.Annals of the rheumatic diseases · 2026Article
- Participation of the purinergic P2X7 receptor in molecular complexes in the nucleus of human chondrocytes.Cellular and molecular life sciences : CMLS · 2026Article
- Tubular epithelial cells promote macrophage pyroptosis through PANX1-extracellular ATP-P2X7 signaling in aldosterone-dependent renal injury.Cell death & disease · 2026Article
- Calcium Pyrophosphate Crystal Formation and Deposition: Where Do we Stand and What Does the Future hold?Current rheumatology reports · 2024Review
- Article
- A Narrative Review of Chondrocalcinosis: Clinical Presentation, Diagnosis, and Therapies.Cureus · 2024Review
- Identification of Common Pathogenic Pathways Involved in Hemochromatosis Arthritis and Calcium Pyrophosphate Deposition Disease: a Review.Current rheumatology reports · 2022Review
- Polycystin-2 Is Required for Chondrocyte Mechanotransduction and Traffics to the Primary Cilium in Response to Mechanical Stimulation.International journal of molecular sciences · 2021Article
- P2X7 Receptor Induces Pyroptotic Inflammation and Cartilage Degradation in Osteoarthritis via NF-Oxidative medicine and cellular longevity · 2021Article
- Restriction of Dietary Phosphate Ameliorates Skeletal Abnormalities in a Mouse Model for Craniometaphyseal Dysplasia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- The membrane protein ANKH is crucial for bone mechanical performance by mediating cellular export of citrate and ATP.PLoS genetics · 2020Article
- Fluorescence Differentiation of ATP-related Multiple Enzymatic Activities in Synovial Fluid as a Marker of Calcium Pyrophosphate Deposition Disease using Kyoto Green.Molecules (Basel, Switzerland) · 2020Article
- Purinergic System Signaling in Metainflammation-Associated Osteoarthritis.Frontiers in medicine · 2020Review
- Signaling of the Purinergic System in the Joint.Frontiers in pharmacology · 2019Review
- Calcium crystal deposition diseases - beyond gout.Nature reviews. Rheumatology · 2018Review
- Cartilage diseases.Matrix biology : journal of the International Society for Matrix Biology · 2018Review
- Review: Unmet Needs and the Path Forward in Joint Disease Associated With Calcium Pyrophosphate Crystal Deposition.Arthritis & rheumatology (Hoboken, N.J.) · 2018Review
- Crystal arthritides - gout and calcium pyrophosphate arthritis : Part 1: Epidemiology and pathophysiology.Zeitschrift fur Gerontologie und Geriatrie · 2018Review
- Mutations in osteoprotegerin account for the CCAL1 locus in calcium pyrophosphate deposition disease.Osteoarthritis and cartilage · 2018Article
- Cell culture: complications due to mechanical release of ATP and activation of purinoceptors.Cell and tissue research · 2017Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
introductionExtracellular ATP (eATP) is released by articular chondrocytes under physiological and pathological conditions. High eATP levels cause pathologic calcification, damage cartilage, and mediate pain. We recently showed that stable over-expression of the progressive ankylosis gene product, ANK, increased chondrocyte eATP levels, but the mechanisms of this effect remained unexplored. The purpose of this work was to further investigate mechanisms of eATP efflux in primary articular chondrocytes and to better define the role of ANK in this process.
methodsWe measured eATP levels using a bioluminescence-based assay in adult porcine articular chondrocyte media with or without a 10 minute exposure to hypotonic stress. siRNAs for known ATP membrane transporters and pharmacologic inhibitors of ATP egress pathways were used to identify participants involved in chondrocyte eATP release.
resultseATP levels increased after exposure to hypotonic media in a calcium-dependent manner in monolayer and 3-dimensional agarose gel cultures (p < 0.001). A potent transient receptor potential vanilloid 4 (TRPV4) agonist mimicked the effects of hypotonic media. ANK siRNA suppressed basal (p < 0.01) and hypotonically-stressed (p < 0.001) ATP levels. This effect was not mediated by altered extracellular pyrophosphate (ePPi) levels, and was mimicked by the ANK inhibitor, probenecid (p < 0.001). The P2X7/4 receptor inhibitor Brilliant Blue G also suppressed eATP efflux induced by hypotonic media (p < 0.001), while ivermectin, a P2X4 receptor stimulant, increased eATP levels (p < 0.001). Pharmacologic inhibitors of hemichannels, maxianion channels and other volume-sensitive eATP efflux pathways did not suppress eATP levels.
conclusionsThese findings implicate ANK and P2X7/4 receptors in chondrocyte eATP efflux. Understanding the mechanisms of eATP efflux may result in novel therapies for calcium crystal arthritis and osteoarthritis.
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