ArticleCartilage2021
Effect of Inflammatory Signaling on Human Articular Chondrocyte Hypertrophy: Potential Involvement of Tissue Repair Macrophages.
Article in Cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Immunomodulatory thermosensitive hydroxypropyl chitin hydrogel platform maintains cartilage-synovium homeostasis for enhanced osteoarthritis therapy.Bioactive materials · 2026Article
- LOXL1, THY1, and TYMS define an annotation-derived hemoglobin-associated immunotranscriptomic signature in osteoarthritis cartilage.Frontiers in immunology · 2026Article
- Deciphering cartilage neuro-immune interactions and innervation profile through 3D engineered osteoarthritic micropathophysiological system.Materials today. Bio · 2025Article
- Article
- TMF suppresses chondrocyte hypertrophy in osteoarthritic cartilage by mediating the FOXO3a/BMPER pathway.Experimental and therapeutic medicine · 2024Article
- Using Macrophage Polarization in Human Platelet Lysate to Test the Immunomodulatory Potential of Cells for Clinical Use.Biomedicines · 2024Article
- Microarchitecture Alternations of Osteochondral Junction in Patients with Osteonecrosis of the Femoral Head.Calcified tissue international · 2024Article
- Collagen type X expression and chondrocyte hypertrophic differentiation during OA and OS development.American journal of cancer research · 2024Review
- Inflammatory and Metabolic Signaling Interfaces of the Hypertrophic and Senescent Chondrocyte Phenotypes Associated with Osteoarthritis.International journal of molecular sciences · 2023Review
- An integrated in silico-in vitro approach for identifying therapeutic targets against osteoarthritis.BMC biology · 2022Article
- Intra-articular injection of triamcinolone acetonide sustains macrophage levels and aggravates osteophytosis during degenerative joint disease in mice.British journal of pharmacology · 2022Article
- Exosomes derived from platelet-rich plasma administration in site mediate cartilage protection in subtalar osteoarthritis.Journal of nanobiotechnology · 2022Article
- Strontium Regulates the Proliferation and Differentiation of Isolated Primary Bovine ChondrocytesFrontiers in pharmacology · 2022Article
- Restraint upon Embryonic MetatarsalInternational journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIn osteoarthritis, chondrocytes tend to acquire a hypertrophic phenotype, which contributes to the modification of the extracellular matrix, resulting in permanent cartilage changes. In mouse chondrocytes, pro-inflammatory macrophages and pro-inflammatory cytokines have been shown to stimulate hypertrophy via the activation of the nuclear factor kappa B (NF-κB) pathway. Whether or not this also occurs in human chondrocytes remains unclear. We therefore aimed to investigate whether hypertrophy-like responses in human cartilage are driven mainly by intrinsic inflammatory signaling or shaped by specific macrophage populations.
designHuman articular chondrocytes were cultured with pro-inflammatory cytokines or medium conditioned by defined macrophage subsets. Furthermore, the effect of inhibition of NF-κB-dependent gene expression was evaluated using the NF-κB inhibitor SC-514. Hypertrophy was assessed by measuring the transcription level of alkaline phosphatase (
resultsThe expression of hypertrophic genes was not promoted in human chondrocytes by pro-inflammatory cytokines neither pro-inflammatory M(IFNγ + TNFα) macrophages. Inhibition of the NF-κB-dependent gene expression did not affect human articular chondrocyte hypertrophy. However, tissue repair M(IL4) macrophages induced hypertrophy by promoting the expression of
conclusionIntrinsic inflammatory signaling activation is not involved in the hypertrophic shift observed in human articular chondrocytes cultured
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