ArticleInternational journal of molecular sciences2014
Matrilin-3 chondrodysplasia mutations cause attenuated chondrogenesis, premature hypertrophy and aberrant response to TGF-β in chondroprogenitor cells.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 25 citations in OpenAlex.
- Suppressing Chondrocyte Hypertrophy to Build Better Cartilage.Bioengineering (Basel, Switzerland) · 2023Review
- Fabrication and Characterization of Layer-by-Layer Janus Base Nano-Matrix to Promote Cartilage Regeneration.Journal of visualized experiments : JoVE · 2022Article
- Controlled Self-Assembly of DNA-Mimicking Nanotubes to Form a Layer-by-Layer Scaffold for Homeostatic Tissue Constructs.ACS applied materials & interfaces · 2021Article
- Matrilin-3-Primed Adipose-Derived Mesenchymal Stromal Cell Spheroids Prevent Mesenchymal Stromal-Cell-Derived Chondrocyte Hypertrophy.International journal of molecular sciences · 2020Article
- Efficacy of matrilin-3-primed adipose-derived mesenchymal stem cell spheroids in a rabbit model of disc degeneration.Stem cell research & therapy · 2020Article
- Genetic Disorders of the Extracellular Matrix.Anatomical record (Hoboken, N.J. : 2007) · 2020Review
- Mice Lacking the Matrilin Family of Extracellular Matrix Proteins Develop Mild Skeletal Abnormalities and Are Susceptible to Age-Associated Osteoarthritis.International journal of molecular sciences · 2020Article
- A novel therapeutic strategy for cartilage diseases based on lipid nanoparticle-RNAi delivery system.International journal of nanomedicine · 2018Article
- The influence of tissue microenvironment on stem cell-based cartilage repair.Annals of the New York Academy of Sciences · 2016Review
- Matrilin-3 Role in Cartilage Development and Osteoarthritis.International journal of molecular sciences · 2016Review
- Potential benefits and limitations of utilizing chondroprogenitors in cell-based cartilage therapy.Connective tissue research · 2015Review
- Matrilin-3 inhibits chondrocyte hypertrophy as a bone morphogenetic protein-2 antagonist.The Journal of biological chemistry · 2014Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Studies have shown that mutations in the matrilin-3 gene (MATN3) are associated with multiple epiphyseal dysplasia (MED) and spondyloepimetaphyseal dysplasia (SEMD). We tested whether MATN3 mutations affect the differentiation of chondroprogenitor and/or mesenchymal stem cells, which are precursors to chondrocytes. ATDC5 chondroprogenitors stably expressing wild-type (WT) MATN3 underwent spontaneous chondrogenesis. Expression of chondrogenic markers collagen II and aggrecan was inhibited in chondroprogenitors carrying the MED or SEMD MATN3 mutations. Hypertrophic marker collagen X remained attenuated in WT MATN3 chondroprogenitors, whereas its expression was elevated in chondroprogenitors expressing the MED or SEMD mutant MATN3 gene suggesting that these mutations inhibit chondrogenesis but promote hypertrophy. TGF-β treatment failed to rescue chondrogenesis markers but dramatically increased collagen X mRNA expression in mutant MATN3 expressing chondroprogenitors. Synovium derived mesenchymal stem cells harboring the SEMD mutation exhibited lower glycosaminoglycan content than those of WT MATN3 in response to TGF-β. Our results suggest that the properties of progenitor cells harboring MATN3 chondrodysplasia mutations were altered, as evidenced by attenuated chondrogenesis and premature hypertrophy. TGF-β treatment failed to completely rescue chondrogenesis but instead induced hypertrophy in mutant MATN3 chondroprogenitors. Our data suggest that chondroprogenitor cells should be considered as a potential target of chondrodysplasia therapy.
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Registered trials
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