ArticlePloS one2017
Post-weaning epiphysiolysis causes distal femur dysplasia and foreshortened hindlimbs in fetuin-A-deficient mice.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 25 citations in OpenAlex.
- SkeletalVis: an exploration and meta-analysis data portal of cross-species skeletal transcriptomics data.Bioinformatics (Oxford, England) · 2019Pooled it
- Constitutive activation of TGF-β receptor type I promotes cortical and cancellous bone formation in adult mice.PloS one · 2026Article
- Sustained release of exogeneous fetuin-A from Hyaluronic acid microplates decreases joint degeneration, synovial hyperplasia and muscle damage in a murine post-traumatic osteoarthritis model.Arthritis research & therapy · 2025Article
- The formation and function of calciprotein particles.Pflugers Archiv : European journal of physiology · 2025Review
- Accelerated Bone Loss in Transgenic Mice Expressing Constitutively Active TGF-β Receptor Type I.International journal of molecular sciences · 2023Article
- Increased UHMWPE Particle-Induced Osteolysis in Fetuin-A-Deficient Mice.Journal of functional biomaterials · 2023Article
- Application of the mineral-binding protein fetuin-A for the detection of calcified lesions.Theranostics · 2023Article
- Tissue chaperoning-the expanded functions of fetuin-A beyond inhibition of systemic calcification.Pflugers Archiv : European journal of physiology · 2022Review
- Fetuin-A and fetal growth in gestational diabetes mellitus.BMJ open diabetes research & care · 2020Article
- Microvasculopathy and soft tissue calcification in mice are governed by fetuin-A, magnesium and pyrophosphate.PloS one · 2020Article
- Lumenal calcification and microvasculopathy in fetuin-A-deficient mice lead to multiple organ morbidity.PloS one · 2020Article
- The role of intra-articular administration of Fetuin-A in post-traumatic knee osteoarthritis: an experimental study in a rat model.Journal of experimental orthopaedics · 2019Article
- Mammalian plasma fetuin-B is a selective inhibitor of ovastacin and meprin metalloproteinases.Scientific reports · 2019Article
- Chemokines in Physiological and Pathological Bone Remodeling.Frontiers in immunology · 2019Review
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetuin-A / α2-Heremans-Schmid-glycoprotein (gene name Ahsg) is a systemic inhibitor of ectopic calcification. Due to its high affinity for calcium phosphate, fetuin-A is highly abundant in mineralized bone matrix. Foreshortened femora in fetuin-A-deficient Ahsg-/- mice indicated a role for fetuin-A in bone formation. We studied early postnatal bone development in fetuin-A-deficient mice and discovered that femora from Ahsg-/- mice exhibited severely displaced distal epiphyses and deformed growth plates, similar to the human disease slipped capital femoral epiphysis (SCFE). The growth plate slippage occurred in 70% of Ahsg-/- mice of both sexes around three weeks postnatal. At this time point, mice weaned and rapidly gained weight and mobility. Epiphysis slippage never occurred in wildtype and heterozygous Ahsg+/- mice. Homozygous fetuin-A-deficient Ahsg-/- mice and, to a lesser degree, heterozygous Ahsg+/- mice showed lesions separating the proliferative zone from the hypertrophic zone of the growth plate. The hypertrophic growth plate cartilage in long bones from Ahsg-/- mice was significantly elongated and V-shaped until three weeks of age and thus prior to the slippage. Genome-wide transcriptome analysis of laser-dissected distal femoral growth plates from 13-day-old Ahsg-/- mice revealed a JAK-STAT-mediated inflammatory response including a 550-fold induction of the chemokine Cxcl9. At this stage, vascularization of the elongated growth plates was impaired, which was visualized by immunofluorescence staining. Thus, fetuin-A-deficient mice may serve as a rodent model of growth plate pathologies including SCFE and inflammatory cartilage degradation.
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