ArticleMolecular and cellular biology2004
Matrilin-3 is dispensable for mouse skeletal growth and development.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 68 citations in OpenAlex.
- Gene Expression Profiling Identifies Two Chordoma Subtypes Associated with Distinct Molecular Mechanisms and Clinical Outcomes.Clinical cancer research : an official journal of the American Association for Cancer Research · 2023Article
- Decorin regulates cartilage pericellular matrix micromechanobiology.Matrix biology : journal of the International Society for Matrix Biology · 2021Article
- Exosomal lncRNA-H19 promotes osteogenesis and angiogenesis through mediating Angpt1/Tie2-NO signaling in CBS-heterozygous mice.Theranostics · 2021Article
- 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
- miR-324-5p is up regulated in end-stage osteoarthritis and regulates Indian Hedgehog signalling by differing mechanisms in human and mouse.Matrix biology : journal of the International Society for Matrix Biology · 2019Article
- Extracellular matrix protein Matrilin-4 regulates stress-induced HSC proliferation via CXCR4.The Journal of experimental medicine · 2016Article
- New therapeutic targets in rare genetic skeletal diseases.Expert opinion on orphan drugs · 2015Article
- Cartilage damage in osteoarthritis and rheumatoid arthritis--two unequal siblings.Nature reviews. Rheumatology · 2015Review
- Matrilin-3 inhibits chondrocyte hypertrophy as a bone morphogenetic protein-2 antagonist.The Journal of biological chemistry · 2014Article
- Extracellular matrix and developing growth plate.Current osteoporosis reports · 2014Review
- Matrilin-1 is essential for zebrafish development by facilitating collagen II secretion.The Journal of biological chemistry · 2014Article
- Derlin-2-deficient mice reveal an essential role for protein dislocation in chondrocytes.Molecular and cellular biology · 2011Article
- Decreased chondrocyte proliferation and dysregulated apoptosis in the cartilage growth plate are key features of a murine model of epiphyseal dysplasia caused by a matn3 mutation.Human molecular genetics · 2007Article
- Neutral sphingomyelinase (SMPD3) deficiency causes a novel form of chondrodysplasia and dwarfism that is rescued by Col2A1-driven smpd3 transgene expression.The American journal of pathology · 2007Article
- Unique matrix structure in the rough endoplasmic reticulum cisternae of pseudoachondroplasia chondrocytes.The American journal of pathology · 2007Article
- Functional knockout of the matrilin-3 gene causes premature chondrocyte maturation to hypertrophy and increases bone mineral density and osteoarthritis.The American journal of pathology · 2006Article
- Altered integration of matrilin-3 into cartilage extracellular matrix in the absence of collagen IX.Molecular and cellular biology · 2005Article
- Zebrafish (Danio rerio) matrilins: shared and divergent characteristics with their mammalian counterparts.The Biochemical journal · 2005Article
- WISP3, the gene responsible for the human skeletal disease progressive pseudorheumatoid dysplasia, is not essential for skeletal function in mice.Molecular and cellular biology · 2005Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Matrilin-3 belongs to the matrilin family of extracellular matrix (ECM) proteins and is primarily expressed in cartilage. Mutations in the gene encoding human matrilin-3 (MATN-3) lead to autosomal dominant skeletal disorders, such as multiple epiphyseal dysplasia (MED), which is characterized by short stature and early-onset osteoarthritis, and bilateral hereditary microepiphyseal dysplasia, a variant form of MED characterized by pain in the hip and knee joints. To assess the function of matrilin-3 during skeletal development, we have generated Matn-3 null mice. Homozygous mutant mice appear normal, are fertile, and show no obvious skeletal malformations. Histological and ultrastructural analyses reveal endochondral bone formation indistinguishable from that of wild-type animals. Northern blot, immunohistochemical, and biochemical analyses indicated no compensatory upregulation of any other member of the matrilin family. Altogether, our findings suggest functional redundancy among matrilins and demonstrate that the phenotypes of MED disorders are not caused by the absence of matrilin-3 in cartilage ECM.
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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.