ArticleThe Journal of biological chemistry2007
Basic fibroblast growth factor stimulates matrix metalloproteinase-13 via the molecular cross-talk between the mitogen-activated protein kinases and protein kinase Cdelta pathways in human adult articular chondrocytes.
Article in The Journal of biological chemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.
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Who cites it
103 citing papers in PubMed, 170 citations in OpenAlex.
- Development and retranslational validation of an in vitro model to characterize acute infections in large human joints.BioMed research international · 2014Trial
- Bovine lactoferricin-induced anti-inflammation is, in part, via up-regulation of interleukin-11 by secondary activation of STAT3 in human articular cartilage.The Journal of biological chemistry · 2013Trial
- Platelet-rich plasma-contained drug delivery systems to treat orthopedic injuries.International journal of pharmaceutics: X · 2025Review
- Targeting Chondrocyte Hypertrophy as Strategies for the Treatment of Osteoarthritis.Bioengineering (Basel, Switzerland) · 2025Review
- The Interplay of Aging and PANoptosis in Osteoarthritis Pathogenesis: Implications for Novel Therapeutic Strategies.Journal of inflammation research · 2025Review
- The Role of Biomarkers in Predicting Outcomes of Anterior Cruciate Ligament Reconstruction: A Systematic Review.Orthopaedic journal of sports medicine · 2024Review
- Role of signaling pathways in age-related orthopedic diseases: focus on the fibroblast growth factor family.Military Medical Research · 2024Review
- The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review.Biomolecules · 2024Review
- Effects and action mechanisms of individual cytokines contained in PRP on osteoarthritis.Journal of orthopaedic surgery and research · 2023Review
- Disrupting mechanical homeostasis promotes matrix metalloproteinase-13 mediated processing of neuron glial antigen 2 in mandibular condylar cartilage.European cells & materials · 2023Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Harnessing Growth Factor Interactions to Optimize Articular Cartilage Repair.Advances in experimental medicine and biology · 2023Review
- Small extracellular vesicles in combination with sleep-related circRNA3503: A targeted therapeutic agent with injectable thermosensitive hydrogel to prevent osteoarthritis.Bioactive materials · 2021Article
- Uncovering pathways regulating chondrogenic differentiation of CHH fibroblasts.Non-coding RNA research · 2021Article
- Methods of Modification of Mesenchymal Stem Cells and Conditions of Their Culturing for Hyaline Cartilage Tissue Engineering.Biomedicines · 2021Review
- Impact of perlecan, a core component of basement membrane, on regeneration of cartilaginous tissues.Acta biomaterialia · 2021Review
- Activation of the extracellular-signal-regulated kinase (ERK)/c-Jun N-terminal kinase (JNK) signal pathway and osteogenic factors in subchondral bone of patients with knee osteoarthritis.Annals of translational medicine · 2021Article
- bFGF-mediated phosphorylation of δ-catenin increases its protein stability and the ability to induce the nuclear redistribution of β-catenin.American journal of cancer research · 2021Article
- Possible Regulation of bFGF Expression by Mast Cells in Osteoarthritis Patients with Obesity: A Cross-Sectional Study.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- Fibroblast growth factor signalling in osteoarthritis and cartilage repair.Nature reviews. Rheumatology · 2020Review
43 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Excessive release of basic fibroblast growth factor (bFGF) during loading and/or injury of the cartilage matrix may contribute to the onset or progression of osteoarthritis. This pathological role may be related to the ability of bFGF to decrease proteoglycan synthesis and to antagonize the activity of anabolic growth factors in cartilage such as insulin-like growth factor-1 and bone morphogenetic protein 7 (BMP7 or OP-1). Matrix metalloproteinase-13 (MMP-13), a catabolic cartilage-degrading enzyme, is dramatically up-regulated by inflammatory cytokines or by fibronectin fragments in articular chondrocytes. In this study, we investigated MMP-13 production by bFGF using human articular chondrocytes. Endogenous concentration of bFGF in synovial fluids collected from arthritis patients and asymptomatic subjects showed a good linear correlation with the endogenous levels of MMP-13. bFGF stimulation of MMP-13 was mediated at the transcriptional level and, at least in part, by stimulation of interleukin-1 production. Also, our findings suggest that bFGF stimulation of MMP-13 required the activation of multiple MAPKs (ERK, p38, and JNK) by bFGF, and more importantly, bFGF activation of protein kinase C (PKC) delta played a key role in the MMP-13 stimulation. Indeed, PKCdelta is the only isoform associated with MMP-13 stimulation among the PKC isoforms tested. PKCdelta controls the bFGF response by regulating multiple MAPK pathways. Our results suggest that PKCdelta activation is a principal rate-limiting event in the bFGF-dependent stimulation of MMP-13 in human adult articular chondrocytes. We propose that deregulation of cross-talk between MAPK and PKCdelta signaling may contribute to the etiology of osteoarthritis in human patients.
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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.