ArticleArthritis and rheumatism2007
Biomechanical signals inhibit IKK activity to attenuate NF-kappaB transcription activity in inflamed chondrocytes.
Article in Arthritis and rheumatism, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 2 of them syntheses that pooled it.
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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
34 citing papers in PubMed, 2 syntheses or guidelines pooled it, 65 citations in OpenAlex.
- Pooled it
- The basic science of continuous passive motion in promoting knee health: a systematic review of studies in a rabbit model.Arthroscopy : the journal of arthroscopic & related surgery : official publication of the Arthroscopy Association of North America and the International Arthroscopy Association · 2013Pooled it
- Exercise induces dynamic changes in intra-articular metabolism and inflammation associated with remodeling of the infrapatellar fat pad in mice.Scientific reports · 2025Article
- Dynamic compression inhibits cytokine-mediated type II collagen degradation.Osteoarthritis and cartilage open · 2022Article
- Mechanisms Underlying Anti-Inflammatory and Anti-Cancer Properties of Stretching-A Review.International journal of molecular sciences · 2022Review
- Combining stretching and gallic acid to decrease inflammation indices and promote extracellular matrix production in osteoarthritic human articular chondrocytes.Experimental cell research · 2021Article
- Review
- Current Trends in the Evaluation of Osteochondral Lesion Treatments: Histology, Histomorphometry, and Biomechanics in Preclinical Models.BioMed research international · 2019Review
- Effect of biomechanical stress on endogenous antioxidant networks in bovine articular cartilage.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2018Article
- Exercise-driven metabolic pathways in healthy cartilage.Osteoarthritis and cartilage · 2016Article
- New developments in the treatment of osteoarthritis - focus on biologic agents.Open access rheumatology : research and reviews · 2015Review
- Role of miR-146a in human chondrocyte apoptosis in response to mechanical pressure injury in vitro.International journal of molecular medicine · 2014Article
- The primary cilium influences interleukin-1β-induced NFκB signalling by regulating IKK activity.Cellular signalling · 2014Article
- Mechanosignaling in bone health, trauma and inflammation.Antioxidants & redox signaling · 2014Review
- Homeostatic mechanisms in articular cartilage and role of inflammation in osteoarthritis.Current rheumatology reports · 2013Review
- Stretching of the back improves gait, mechanical sensitivity and connective tissue inflammation in a rodent model.PloS one · 2012Article
- Biomechanical factors in osteoarthritis.Best practice & research. Clinical rheumatology · 2011Review
- Mechanotransduction and cartilage integrity.Annals of the New York Academy of Sciences · 2011Review
- Mechanical loading: bone remodeling and cartilage maintenance.Current osteoporosis reports · 2011Review
- Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveWhile the effects of biomechanical signals in the form of joint movement and exercise are known to be beneficial to inflamed joints, limited information is available regarding the intracellular mechanisms of their actions. This study was undertaken to examine the intracellular mechanisms by which biomechanical signals suppress proinflammatory gene induction by the interleukin-1-beta (IL-1beta)-induced NF-kappaB signaling cascade in articular chondrocytes.
methodsPrimary rat articular chondrocytes were exposed to biomechanical signals in the form of cyclic tensile strain, and the effects on the NF-kappaB signaling cascade were examined by Western blot analysis, real-time polymerase chain reaction, and immunofluorescence.
resultsCyclic tensile strain rapidly inhibited the IL-1beta-induced nuclear translocation of NF-kappaB, but not its IL-1beta-induced phosphorylation at serine 276 and serine 536, which are necessary for its transactivation and transcriptional efficacy, respectively. Examination of upstream events revealed that cyclic tensile strain also inhibited the cytoplasmic protein degradation of IkappaBbeta and IkappaBalpha, as well as repressed their gene transcription. Additionally, cyclic tensile strain induced a rapid nuclear translocation of IkappaBalpha to potentially prevent NF-kappaB binding to DNA. Furthermore, the inhibition of IL-1beta-induced degradation of IkappaB by cyclic tensile strain was mediated by down-regulation of IkappaB kinase activity.
conclusionThese results indicate that the signals generated by cyclic tensile strain act at multiple sites within the NF-kappaB signaling cascade to inhibit IL-1beta-induced proinflammatory gene induction. Taken together, these findings provide insight into how biomechanical signals regulate and reduce inflammation, and underscore their potential in enhancing the ability of chondrocytes to curb inflammation in diseased joints.
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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.