ArticleOsteoarthritis and cartilage2021
Transcriptional response of human articular chondrocytes treated with fibronectin fragments: an in vitro model of the osteoarthritis phenotype.
Article in Osteoarthritis and cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 37 citations in OpenAlex.
- Osteoarthritic synovial fibroblasts drive inflammatory responses and impair chondrocyte function in response to a fibronectin matrikine.Osteoarthritis and cartilage · 2026Article
- CSPG4Osteoarthritis and cartilage open · 2026Article
- Vasoactive intestinal peptide advances chondrogenesis and modulates pathogenic mediators in human osteoarthritis.Journal of molecular medicine (Berlin, Germany) · 2026Article
- Research progress on the mechanism of chondrocyte ferroptosis in osteoarthritis.Frontiers in immunology · 2026Review
- From mechanism to medicine: The progress and potential of epigenetics in osteoarthritis.Osteoarthritis and cartilage open · 2025Review
- Evaluating the role of lipopolysaccharides in the joint: fibronectin as a novel protective mechanism.RMD open · 2025Article
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- Matrikine stimulation of equine synovial fibroblasts and chondrocytes results in an in vitro osteoarthritis phenotype.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.Cell genomics · 2025Article
- Enhanced therapeutic potential of a self-healing hyaluronic acid hydrogel for early intervention in osteoarthritis.Materials today. Bio · 2024Article
- Response splicing QTLs in primary human chondrocytes identifies putative osteoarthritis risk genes.bioRxiv : the preprint server for biology · 2024Article
- Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.bioRxiv : the preprint server for biology · 2024Article
- Effect of Passaging on Bovine Chondrocyte Gene Expression and Engineered Cartilage Production.Tissue engineering. Part A · 2024Article
- Integrin signalling in joint development, homeostasis and osteoarthritis.Nature reviews. Rheumatology · 2024Review
- Primary osteoarthritis chondrocyte map of chromatin conformation reveals novel candidate effector genes.Annals of the rheumatic diseases · 2024Article
- Spatial analysis of the osteoarthritis microenvironment: techniques, insights, and applications.Bone research · 2024Review
- A novel small molecule screening assay using normal human chondrocytes toward osteoarthritis drug discovery.PloS one · 2024Article
- Epigenetics as a mediator of genetic risk in osteoarthritis: role during development, homeostasis, aging, and disease progression.American journal of physiology. Cell physiology · 2023Review
- Identification and functional characterization of imbalanced osteoarthritis-associated fibronectin splice variants.Rheumatology (Oxford, England) · 2023Article
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Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveFibronectin is a matrix protein that is fragmented during cartilage degradation in osteoarthritis (OA). Treatment of chondrocytes with fibronectin fragments (FN-f) has been used to model OA in vitro, but the system has not been fully characterized. This study sought to define the transcriptional response of chondrocytes to FN-f, and directly compare it to responses traditionally observed in OA.
designNormal human femoral chondrocytes isolated from tissue donors were treated with either FN-f or PBS (control) for 3, 6, or 18 h. RNA-seq libraries were compared between time-matched FN-f and control samples in order to identify changes in gene expression over time. Differentially expressed genes were compared to a published OA gene set and used for pathway, transcription factor motif, and kinome analysis.
resultsFN-f treatment resulted in 3,914 differentially expressed genes over the time course. Genes that are up- or downregulated in OA were significantly up- (P < 0.00001) or downregulated (P < 0.0004) in response to FN-f. Early response genes were involved in proinflammatory pathways, whereas many late response genes were involved in ferroptosis. The promoters of upregulated genes were enriched for NF-κB, AP-1, and IRF motifs. Highly upregulated kinases included CAMK1G, IRAK2, and the uncharacterized kinase DYRK3, while growth factor receptors TGFBR2 and FGFR2 were downregulated.
conclusionsFN-f treatment of normal human articular chondrocytes recapitulated many key aspects of the OA chondrocyte phenotype. This in vitro model is promising for future OA studies, especially considering its compatibility with genomics and genome-editing techniques.
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Registered trials
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