ArticleThe American journal of pathology2006
Functional knockout of the matrilin-3 gene causes premature chondrocyte maturation to hypertrophy and increases bone mineral density and osteoarthritis.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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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.
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Who cites it
42 citing papers in PubMed, 109 citations in OpenAlex.
- Borderline acceleration in blood epigenetic age of unclear biological importance in knee osteoarthritis progression: Specimens and data from the Osteoarthritis Initiative and Johnston County Osteoarthritis Project.Osteoarthritis and cartilage · 2026Article
- Phased-assembly-driven pangenome graphs for structural variant genotyping and complex trait mapping in dairy cattle.Nature communications · 2026Article
- Application of a French cattle pangenome, from structural variant discovery to association studies on key phenotypes.Genetics, selection, evolution : GSE · 2025Article
- Development of a Mouse Model of Enthesis-Specific NF-κB Activation.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Differentiation of Hypertrophic Chondrocytes from Human iPSCs for the In Vitro Modeling of Chondrodysplasias.Stem cell reports · 2021Article
- Matrilin-3-Primed Adipose-Derived Mesenchymal Stromal Cell Spheroids Prevent Mesenchymal Stromal-Cell-Derived Chondrocyte Hypertrophy.International journal of molecular sciences · 2020Article
- Inner histopathologic changes and disproportionate zone volumes in foetal growth plates following gestational hypoglycaemia in rats.Scientific reports · 2020Article
- 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
- Electrospun Polymers in Cartilage Engineering-State of Play.Frontiers in bioengineering and biotechnology · 2020Review
- Comparative analysis demonstrates cell type-specific conservation of SOX9 targets between mouse and chicken.Scientific reports · 2019Article
- The distribution patterns of COMP and matrilin-3 in septal, alar and triangular cartilages of the human nose.Histochemistry and cell biology · 2018Article
- Suppressing mesenchymal stem cell hypertrophy and endochondral ossification in 3D cartilage regeneration with nanofibrous poly(l-lactic acid) scaffold and matrilin-3.Acta biomaterialia · 2018Article
- Recent Insights into the Contribution of the Changing Hypertrophic Chondrocyte Phenotype in the Development and Progression of Osteoarthritis.Frontiers in bioengineering and biotechnology · 2018Review
- Extracellular Distribution of Collagen II and Perifibrillar Adapter Proteins in Healthy and Osteoarthritic Human Knee Joint Cartilage.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2017Article
- Clinical significance of Matrilin-3 gene polymorphism in Egyptian patients with primary knee osteoarthritis.European journal of rheumatology · 2017Article
- Intra-articular Delivery of Antago-miR-483-5p Inhibits Osteoarthritis by Modulating Matrilin 3 and Tissue Inhibitor of Metalloproteinase 2.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Matrilin-3 Role in Cartilage Development and Osteoarthritis.International journal of molecular sciences · 2016Review
- Drug-induced regeneration in adult mice.Science translational medicine · 2015Article
- Novel insights into the function and dynamics of extracellular matrix in liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2015Review
- Regulation of α5 and αV Integrin Expression by GDF-5 and BMP-7 in Chondrocyte Differentiation and Osteoarthritis.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Mutations in the gene encoding matrilin-3 (MATN3), a noncollagenous extracellular matrix protein, have been reported in a variety of skeletal diseases, including multiple epiphyseal dysplasia, which is characterized by irregular ossification of the epiphyses and early-onset osteoarthritis, spondylo-epimetaphyseal dysplasia, and idiopathic hand osteoarthritis. To assess the role of matrilin-3 in the pathogenesis of these diseases, we generated Matn3 functional knockout mice using embryonic stem cell technology. In the embryonic growth plate of the developing long bones, Matn3 null chondrocytes prematurely became prehypertrophic and hypertrophic, forming an expanded zone of hypertrophy. This expansion was attenuated during the perinatal period, and Matn3 homozygous null mice were viable and showed no gross skeletal malformations at birth. However, by 18 weeks of age, Matn3 null mice had a significantly higher total body bone mineral density than Matn1 null mice or wild-type littermates. Aged Matn3 null mice were much more predisposed to develop severe osteoarthritis than their wild-type littermates. Here, we show that matrilin-3 plays a role in modulating chondrocyte differentiation during embryonic development, in controlling bone mineral density in adulthood, and in preventing osteoarthritis during aging. The lack of Matn3 does not lead to postnatal chondrodysplasia but accounts for higher incidence of osteoarthritis.
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