ArticleProceedings of the National Academy of Sciences of the United States of America2014
Cartilage-specific deletion of Mig-6 results in osteoarthritis-like disorder with excessive articular chondrocyte proliferation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- The role of the HB-EGF-regulated EGFR-mitophagy axis in maintaining cartilage homeostasis and osteoarthritis.Journal of molecular histology · 2026Article
- Calycosin ameliorates osteoarthritis by regulating the imbalance between chondrocyte synthesis and catabolism.BMC complementary medicine and therapies · 2024Article
- RNA-binding proteins in bone pathophysiology.Frontiers in cell and developmental biology · 2024Review
- Investigation of the efficacy of epidermal growth factor, boric acid and their combination in cartilage injury in rats: An experimental study.Joint diseases and related surgery · 2024Article
- Anabolic phenotype in cartilage-specific mitogen-inducible gene-6 knockout mice is independent of transforming growth factor-α.Osteoarthritis and cartilage open · 2023Article
- Pancreatic loss of Mig6 alters murine endocrine cell fate and protects functional beta cell mass in an STZ-induced model of diabetes.bioRxiv : the preprint server for biology · 2023Article
- Epidermal growth factor signalling pathway in endochondral ossification: an evidence-based narrative review.Annals of medicine · 2022Review
- Activating EGFR Signaling Attenuates Osteoarthritis Development Following Loading Injury in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- EGFR Signaling Is Required for Maintaining Adult Cartilage Homeostasis and Attenuating Osteoarthritis Progression.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- Single-nucleotide polymorphisms as important risk factors of diabetes among Middle East population.Human genomics · 2022Review
- Pharmaceutical therapeutics for articular regeneration and restoration: state-of-the-art technology for screening small molecular drugs.Cellular and molecular life sciences : CMLS · 2021Review
- miR-7/EGFR/MEGF9 axis regulates cartilage degradation in osteoarthritis via PI3K/AKT/mTOR signaling pathway.Bioengineered · 2021Article
- Gene 33/Mig6/ERRFI1, an Adapter Protein with Complex Functions in Cell Biology and Human Diseases.Cells · 2021Review
- Targeting cartilage EGFR pathway for osteoarthritis treatment.Science translational medicine · 2021Article
- EGFR Signaling: Friend or Foe for Cartilage?JBMR plus · 2019Review
- The Role of ERRFI1+808T/G Polymorphism in Diabetic Nephropathy.International journal of molecular and cellular medicine · 2019Article
- Lin28a overexpression reveals the role of Erk signaling in articular cartilage development.Development (Cambridge, England) · 2018Article
- Gefitinib for Epidermal Growth Factor Receptor Activated Osteoarthritis Subpopulation Treatment.EBioMedicine · 2018Article
- FoxO transcription factors modulate autophagy and proteoglycan 4 in cartilage homeostasis and osteoarthritis.Science translational medicine · 2018Article
- RNA-binding protein SAMD4 regulates skeleton development through translational inhibition of Mig6 expression.Cell discovery · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A deficiency of mitogen-inducible gene-6 (Mig-6) in mice leads to the development of an early-onset, osteoarthritis (OA)-like disorder in multiple synovial joints, underlying its importance in maintaining joint homeostasis. Here we determined what joint tissues Mig-6 is expressed in and what role chondrocytes play in the Mig-6-deficient OA-like disorder. A Mig-6/lacZ reporter mouse strain expressing β-galactosidase under the control of the Mig-6 gene promoter was generated to determine Mig-6 expression in joint tissues. By β-galactosidase staining, we demonstrated that Mig-6 was uniquely expressed in the cells across the entire surface of the synovial joint cavity, including chondrocytes in the superficial zone of articular cartilage and in the meniscus, as well as synovial lining cells. By crossing Mig-6-floxed mice to Col2a1-Cre transgenic mice, to generate cartilage-specific deletion of Mig-6, we demonstrated that deficiency of Mig-6 in the chondrocytes results in a joint phenotype that only partially recapitulates the OA-like disorder of the Mig-6-deficient mice: Ubiquitous deletion of Mig-6 led to the OA-like disorder in multiple joints, whereas cartilage-specific deletion affected the knees but rarely other joints. Furthermore, chondrocytes with Mig-6 deficiency showed excessive proliferative activities along with enhanced EGF receptor signaling in the articular cartilage and in the abnormally formed osteophytes. Our findings provide insight into the crucial requirement for Mig-6 in maintaining joint homeostasis and in regulating chondrocyte activities in the synovial joints. Our data also suggest that other cell types are required for fully developing the Mig-6-deficient OA-like disorder.
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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.