ArticleArthritis and rheumatism2012
Time-series transcriptional profiling yields new perspectives on susceptibility to murine osteoarthritis.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 61 citations in OpenAlex.
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- The Age-dependent Influence of the Infrapatellar Fat Pad on Chondrocyte Extracellular Matrix Production.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
- A synoptic literature review of animal models for investigating the biomechanics of knee osteoarthritis.Frontiers in bioengineering and biotechnology · 2024Review
- 3D profiling of mouse epiphyses across ages reveals new potential imaging biomarkers of early spontaneous osteoarthritis.Journal of anatomy · 2023Article
- An integrated in silico-in vitro approach for identifying therapeutic targets against osteoarthritis.BMC biology · 2022Article
- Structural clues to articular calcified cartilage function: A descriptive review of this crucial interface tissue.Journal of anatomy · 2022Review
- High bone mass in mice can be linked to lower osteoclast formation, resorptive capacity, and restricted in vitro sensitivity to inhibition by stable sulforaphane.Cell biochemistry and function · 2022Article
- Characterization of Non-Invasively Induced Post-Traumatic Osteoarthritis in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Degenerative Joint Damage Is Not a Risk Factor for Streptococcal Sepsis and Septic Arthritis in Mice.Life (Basel, Switzerland) · 2021Article
- Pathogenesis of Osteoarthritis: Risk Factors, Regulatory Pathways in Chondrocytes, and Experimental Models.Biology · 2020Review
- Meniscal and ligament modifications in spontaneous and post-traumatic mouse models of osteoarthritis.Arthritis research & therapy · 2020Article
- RSK-3 promotes cartilage regeneration via interacting with rpS6 in cartilage stem/progenitor cells.Theranostics · 2020Article
- Naturally occurring osteoarthritis in male mice with an extended lifespan.Connective tissue research · 2020Article
- Identification of transcription factors responsible for dysregulated networks in human osteoarthritis cartilage by global gene expression analysis.Osteoarthritis and cartilage · 2018Article
- Sexually dimorphic tibia shape is linked to natural osteoarthritis in STR/Ort mice.Osteoarthritis and cartilage · 2018Article
- Article
- The STR/ort mouse model of spontaneous osteoarthritis - an update.Osteoarthritis and cartilage · 2017Review
- Models to define the stages of articular cartilage degradation in osteoarthritis development.International journal of experimental pathology · 2017Review
- Increased Activity of the Chondrocyte Translational Apparatus Accompanies Osteoarthritic Changes in Human and Rodent Knee Cartilage.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
objectiveChronological age is a powerful epidemiologic risk factor for osteoarthritis (OA), a multifactorial disease that is characterized by articular cartilage (AC) degradation. It is unclear from a molecular perspective how aging interacts with OA to produce this risk to AC integrity. To address this key question, we used in vivo time-course analysis of OA development and murine interstrain variability in natural susceptibility to OA to examine changes in non-OA-prone CBA mice versus OA-prone STR/Ort mice, which develop disease that bears significant histologic resemblance to human OA. Through global transcriptome profiling, we attempted to discover the molecular signature linked with both OA vulnerability and progression.
methodsAffymetrix Mouse Gene 1.0 ST Array profiles were generated from AC samples derived from CBA and STR/Ort mice at 3 different ages, corresponding to the stages prior to, at, and late after the natural onset of OA in the STR/Ort mice.
resultsWe found that the OA in STR/Ort mice exhibited a molecular phenotype resembling human OA, and we pinpointed a central role of NF-κB signaling and the emergence of an immune-related signature in OA cartilage over time. We discovered that, strikingly, young healthy AC has a highly expressed skeletal muscle gene expression program, which is switched off during maturation, but is intriguingly retained in AC during OA development in STR/Ort mice.
conclusionThis study is the first to show that AC chondrocytes share a high-abundance gene-expression program with skeletal muscle. We show that failure to switch this program off, as well as the restoration of this program, is associated with inappropriate expression of NF-κB signaling pathways, skeletal muscle-related genes, and induction and/or progression of OA.
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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.