ArticleArthritis research & therapy2005
Octacalcium phosphate crystals directly stimulate expression of inducible nitric oxide synthase through p38 and JNK mitogen-activated protein kinases in articular chondrocytes.
Article in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Systematic Overview of Solid Particles and Their Host Responses.Frontiers in immunology · 2018Pooled it
- Pterostilbene Protects against Osteoarthritis through NLRP3 Inflammasome Inactivation and Improves Gut Microbiota as Evidenced byJournal of agricultural and food chemistry · 2024Article
- Glycolysis: an emerging regulator of osteoarthritis.Frontiers in immunology · 2023Review
- Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification.Pflugers Archiv : European journal of physiology · 2022Review
- Multiple proliferation signaling pathways are modulated by octacalcium phosphate in osteoblasts.International journal of medical sciences · 2022Article
- Review
- Adsorption of Serum Albumin onto Octacalcium Phosphate in Supersaturated Solutions Regarding Calcium Phosphate Phases.Materials (Basel, Switzerland) · 2019Article
- Calcification of the acetabular labrum of the hip: prevalence in the general population and relation to hip articular cartilage and fibrocartilage degeneration.Arthritis research & therapy · 2018Article
- Cartilage calcification of the ankle joint is associated with osteoarthritis in the general population.BMC musculoskeletal disorders · 2018Article
- Calcium-Containing Crystals and Osteoarthritis: an Unhealthy Alliance.Current rheumatology reports · 2018Review
- Inflammatory Potential of Four Different Phases of Calcium Pyrophosphate Relies on NF-κB Activation and MAPK Pathways.Frontiers in immunology · 2018Article
- A wogonin-rich-fraction of Scutellaria baicalensis root extract exerts chondroprotective effects by suppressing IL-1β-induced activation of AP-1 in human OA chondrocytes.Scientific reports · 2017Article
- Biological Effects of Phosphocitrate on Osteoarthritic Articular Chondrocytes.The open rheumatology journal · 2017Article
- Sodium Thiosulfate Prevents Chondrocyte Mineralization and Reduces the Severity of Murine Osteoarthritis.PloS one · 2016Article
- Disease-modifying effects of phosphocitrate and phosphocitrate-β-ethyl ester on partial meniscectomy-induced osteoarthritis.BMC musculoskeletal disorders · 2015Article
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- The role of Syk in osteoarthritis.Clinical immunology (Orlando, Fla.) · 2012Article
- Crystals, inflammation, and osteoarthritis.Current opinion in rheumatology · 2011Review
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Basic calcium phosphate (BCP) crystals, including hydroxyapatite, octacalcium phosphate (OCP) and carbonate-apatite, have been associated with severe osteoarthritis and several degenerative arthropathies. Most studies have considered the chondrocyte to be a bystander in the pathogenesis of calcium crystal deposition disease, assuming that synovial cell cytokines were the only triggers of chondrocyte activation. In the present study we identified direct activation of articular chondrocytes by OCP crystals, which are the BCP crystals with the greatest potential for inducing inflammation. OCP crystals induced nitric oxide (NO) production and inducible nitric oxide synthase (NOS) mRNA expression by isolated articular chondrocytes and cartilage fragments, in a dose-dependent manner and with variations over time. OCP crystals also induced IL-1beta mRNA expression. Using pharmacological and cytokine inhibitors, we observed that OCP crystals induced NO production and inducible NOS mRNA activation were regulated at both the transcriptional and the translational levels; were independent from IL-1beta gene activation; and involved p38 and c-Jun amino-terminal kinase (JNK) mitogen-activated protein kinase (MAPK) pathways, as further confirmed by OCP crystal-induced p38 and JNK MAPK phosphorylation. Taken together, our data suggest that the transcriptional inducible NOS response to OCP crystals involved both the p38 and the JNK MAPK pathways, probably under the control of activator protein-1. NO, a major mediator of cartilage degradation, can be directly produced by BCP crystals in chondrocytes. Together with synovial activation, this direct mechanism may be important in the pathogenesis of destructive arthropathies triggered by microcrystals.
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Registered trials
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