ArticleAmerican journal of physiology. Cell physiology2009
Titanium particles stimulate COX-2 expression in synovial fibroblasts through an oxidative stress-induced, calpain-dependent, NF-kappaB pathway.
Article in American journal of physiology. Cell physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- The immune-microbe-metal triad: a vicious cycle driving biomaterial corrosion in the oral inflammatory microenvironment.Bioactive materials · 2027Review
- Gut microbiota in chronic inflammation: the interplay with lipid mediators.Gut microbes · 2026Review
- Effect of cobalt ions on TNF-α and IL-6 secretion by fibroblasts surrounding hip periprosthetic membrane.Frontiers in bioengineering and biotechnology · 2025Article
- Byakangelicol suppresses TiPs-stimulated osteoclastogenesis and bone destruction via COX-2/NF-κB signaling pathway.Regenerative biomaterials · 2024Article
- Tumor protein P63 Regulated 1 contributes to inflammation and cell proliferation of cystitis glandularis through regulating the NF-кB/cyclooxygenase-2/prostaglandin E2 axis.Bosnian journal of basic medical sciences · 2022Article
- Dental and Orthopaedic Implant Loosening: Overlap in Gene Expression Regulation.Frontiers in immunology · 2022Article
- Tolerogenic dendritic cells suppress titanium particle-induced inflammation.Experimental and therapeutic medicine · 2021Article
- Fibroblast-like cells change gene expression of bone remodelling markers in transwell cultures.European journal of medical research · 2020Article
- Titanium Ions Play a Synergistic Role in the Activation of NLRP3 Inflammasome in Jurkat T Cells.Inflammation · 2020Article
- Article
- Strontium inhibits titanium particle-induced osteoclast activation and chronic inflammation via suppression of NF-κB pathway.Scientific reports · 2016Article
- Majoon ushba, a polyherbal compound, suppresses pro-inflammatory mediators and RANKL expression via modulating NFкB and MAPKs signaling pathways in fibroblast-like synoviocytes from adjuvant-induced arthritic rats.Immunologic research · 2016Article
- μ-Calpain as a Novel Target for Impairment of Nitric Oxide-Mediated Vascular Relaxation in Diabetes: A Mini Review.Journal of molecular and genetic medicine : an international journal of biomedical research · 2015Article
- Comparison of the cytotoxic and inflammatory responses of titanium particles with different methods for endotoxin removal in RAW264.7 macrophages.Journal of materials science. Materials in medicine · 2012Article
- Index radial collateral ligament repair with titanium mini-suture anchor: osteolysis complication of an underreported injury.Hand (New York, N.Y.) · 2010Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
In prosthetic loosening, bone resorption is induced by wear debris particles generated from the artificial joint articulation. Our prior work showed that synovial-like fibroblasts respond to titanium particles by producing receptor activator of NF-kappaB ligand (RANKL), a critical activator of osteoclastogenesis. While this effect occurs through a cyclooxygenase-2 (COX-2)-dependent pathway, the mechanism of COX-2 stimulation by titanium particles is not clear. Here we show that titanium particles induce COX-2 gene expression by activating NF-kappaB signaling. Inhibitor of NF-kappaB (IkappaBalpha) is degraded following particle treatment, permitting active NF-kappaB to translocate to the nucleus where it interacts with the COX-2 promoter and drives transcription. NF-kappaB activation is dependent on reactive oxygen species since antioxidants block the NF-kappaB signaling induced by particles. Surprisingly, IkappaBalpha degradation is independent of IKK (IkappaB kinase) and the 26S proteasome. Instead, calpain inhibitor can block the IkappaBalpha degradation induced by particles. Furthermore, the calpain-targeted COOH-terminal PEST sequence of IkappaBalpha is necessary for phosphorylation and degradation, consistent with a proteasome-independent mechanism of catabolism. Altogether, the data demonstrate a signaling pathway by which titanium particles induce oxidative stress, stimulate calpain-mediated NF-kappaB activation, and activate target gene expression, including COX-2. These findings define important targets for osteolysis but may also have importance in other diseases where fibroblasts respond to environmental particles, including pulmonary diseases.
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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.