ArticleArthritis & rheumatology (Hoboken, N.J.)2017
Increased Activity of the Chondrocyte Translational Apparatus Accompanies Osteoarthritic Changes in Human and Rodent Knee Cartilage.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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
14 citing papers in PubMed, 26 citations in OpenAlex.
- Ribosome heterogeneity and specialization in musculoskeletal physiology and pathology.JBMR plus · 2026Article
- Targeting mTOR in Systemic Lupus Erythematosus: From Immune Cell Dysfunction to Clinical Translation.Journal of inflammation research · 2026Review
- ChemPert: mapping between chemical perturbation and transcriptional response for non-cancer cells.Nucleic acids research · 2023Article
- Ribosome dysfunction in osteoarthritis.Current opinion in rheumatology · 2022Review
- Emerging pharmaceutical therapeutics and delivery technologies for osteoarthritis therapy.Frontiers in pharmacology · 2022Review
- Identification of circRNA Expression Profiles in BMSCs from Glucocorticoid-Induced Osteoporosis Model.Stem cells international · 2022Article
- Synovial Macrophages in Osteoarthritis: The Key to Understanding Pathogenesis?Frontiers in immunology · 2021Review
- Gene Expression in Meniscal Tears at the Time of Arthroscopic Partial Meniscectomy Predicts the Progression of Osteoarthritis Within 6 Years of Surgery.Orthopaedic journal of sports medicine · 2020Article
- Pathomechanisms of Posttraumatic Osteoarthritis: Chondrocyte Behavior and Fate in a Precarious Environment.International journal of molecular sciences · 2020Review
- Periostin interaction with discoidin domain receptor-1 (DDR1) promotes cartilage degeneration.PloS one · 2020Article
- Translational regulation contributes to the secretory response of chondrocytic cells following exposure to interleukin-1β.The Journal of biological chemistry · 2019Article
- LncRNA MALAT1 promotes osteoarthritis by modulating miR-150-5p/AKT3 axis.Cell & bioscience · 2019Review
- 29-kDa FN-f inhibited autophagy through modulating localization of HMGB1 in human articular chondrocytes.BMB reports · 2018Article
- Stratification of knee osteoarthritis: two major patient subgroups identified by genome-wide expression analysis of articular cartilage.Annals of the rheumatic diseases · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
objectiveDegeneration of articular cartilage is central to the pathology of osteoarthritis (OA). However, the molecular mechanisms leading to these irreversible changes are still poorly understood. This study was undertaken to investigate how changes in the chondrocyte translational apparatus may contribute to the development and progression of knee OA.
methodsArticular cartilage from the knees of normal healthy subjects and patients with OA was used to analyze the activity of different components of the translational machinery. Chondrocytes isolated from lesional and nonlesional areas of the human OA cartilage were used to estimate the relative rate of protein synthesis by metabolic labeling. Experimental OA was induced by transection of the anterior cruciate ligament of rats to investigate changes in the translational apparatus associated with OA. The role of interleukin-1β (IL-1β) signaling was assessed in vitro using rat articular chondrocytes. In human or rodent knee cartilage, messenger RNA expression was analyzed by quantitative polymerase chain reaction, and protein levels were determined by immunohistochemistry and Western blotting.
resultsSeveral novel traits of OA chondrocytes were identified, including up-regulation of the serine/threonine kinases Akt-2 and Akt-3 at the posttranscriptional level and an increased rate of total protein synthesis, likely attributable to inactivation of eukaryotic initiation factor 4E binding protein 1 (4E-BP1), a known repressor of cap-dependent translation. Inactivation of 4E-BP1 was dependent on the activity of mechanistic target of rapamycin and was crucial for the up-regulation of protein synthesis in general and expression of matrix metalloproteinase 13 and ADAMTS-5 in particular. In addition, treatment of articular chondrocytes with IL-1β led to inactivation of 4E-BP1 and up-regulation of protein synthesis.
conclusionPrecise control of protein synthesis is vital for cartilage homeostasis, and its dysregulation contributes to the molecular pathology of OA. The results of this study therefore identify a novel set of potential therapeutic targets to ameliorate the effects of knee OA.
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