ArticleJournal of bone and mineral metabolism2017
Novel role of CCN3 that maintains the differentiated phenotype of articular cartilage.
Article in Journal of bone and mineral metabolism, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- The Relationship Between CCN3 and Rheumatoid Arthritis and Its Potential Therapeutic Value.Journal of immunology research · 2026Review
- Association of organs-crosstalk with the pathogenesis of osteoarthritis: cartilage as a key player.Frontiers in endocrinology · 2025Review
- An Equine Protein Atlas Highlights Synovial Fluid Proteome Dynamics during Experimentally LPS-Induced Arthritis.Journal of proteome research · 2024Article
- Dual roles of cellular communication network factor 6 (CCN6) in the invasion and metastasis of oral cancer cells to bone via binding to BMP2 and RANKL.Carcinogenesis · 2023Article
- Do not overwork: cellular communication network factor 3 for life in cartilage.Journal of cell communication and signaling · 2023Review
- Molecular and Genetic Interactions between CCN2 and CCN3 behind Their Yin-Yang Collaboration.International journal of molecular sciences · 2022Review
- Modeling cartilage pathology in mucopolysaccharidosis VI using iPSCs reveals early dysregulation of chondrogenic and metabolic gene expression.Frontiers in bioengineering and biotechnology · 2022Article
- CCN proteins in the musculoskeletal system: current understanding and challenges in physiology and pathology.Journal of cell communication and signaling · 2021Review
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- Tissue Engineering Strategies to Increase Osteochondral Regeneration of Stem Cells; a Close Look at Different Modalities.Stem cell reviews and reports · 2021Review
- Targeting CCN Proteins in Rheumatoid Arthritis and Osteoarthritis.International journal of molecular sciences · 2021Review
- The Emerging Roles of CCN3 Protein in Immune-Related Diseases.Mediators of inflammation · 2021Review
- Higher Serum CCN3 Is Associated with Disease Activity and Inflammatory Markers in Rheumatoid Arthritis.Journal of immunology research · 2020Article
- NOV/CCN3 induces cartilage protection by inhibiting PI3K/AKT/mTOR pathway.Journal of cellular and molecular medicine · 2019Article
- Roles of matricellular CCN2 deposited by osteocytes in osteoclastogenesis and osteoblast differentiation.Scientific reports · 2019Article
- Possible reparative effect of low-intensity pulsed ultrasound (LIPUS) on injured meniscus.Journal of cell communication and signaling · 2019Article
- A friend in knee: CCN3 may inhibit osteoarthritis progression.Journal of cell communication and signaling · 2018Article
- Metabolic regulation of the CCN family genes by glycolysis in chondrocytes.Journal of cell communication and signaling · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Knowledge of the microenvironment of articular cartilage in health and disease is the key to accomplishing fundamental disease-modifying treatments for osteoarthritis. The proteins comprising the CCN Family are matricellular proteins with a remarkable relevance within the context of cartilage metabolism. CCN2 displays a great capability for regenerating articular cartilage, and CCN3 has been shown to activate the expression of genes related to articular chondrocytes and to repress genes related to endochondral ossification in epiphyseal chondrocytes. Moreover, mice lacking CCN3 protein have been shown to display ostearthritic changes in their knee articular cartilage. In this study, we employed a monoiodoacetic acid (MIA)-induced osteoarthritic model to investigate whether osteoarthritic changes in the cartilage are reciprocally accompanied by CCN3 down-regulation and an inducible overexpression system to evaluate the effects of CCN3 on articular chondrocytes in vitro. Finally, we also investigated the effects of exogenous CCN3 in vivo during the early stages of MIA-induced osteoarthritis. We discovered that CCN3 is expressed by articular chondrocytes in normal rat knees, whereas it is rapidly down-regulated in osteoarthritic knees. In vitro, we also discovered that CCN3 increases the proteoglycan accumulation, the gene expression of type II collagen, tenascin-C and lubricin, as well as the protein production of tenascin-C and lubricin in articular chondrocytes. In vivo, it was discovered that exogenous CCN3 increased tidemark integrity and produced an increased production of lubricin protein. The potential utility of CCN3 as a future therapeutic agent and possible strategies to improve its therapeutic functions are also discussed.
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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 Socratic graph.