ArticleCalcified tissue international2013
Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent.
Article in Calcified tissue international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 57 citations in OpenAlex.
- ERK-Mediated Phosphorylation of YAP Defines a Noncanonical FGF Signaling Mechanism in Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Initial In Vivo Analyses of Small Pore Polymer Scaffolds for Creation of an Artificial Cranial Stem Cell Niche.Bioengineering (Basel, Switzerland) · 2026Article
- Regional variability in craniofacial stiffness: a study in normal and Crouzon mice during postnatal development.Biomechanics and modeling in mechanobiology · 2025Article
- Cyclic loading failed to promote growth in a pig model of midfacial hypoplasia.Journal of anatomy · 2024Article
- Cranial bone microarchitecture in a mouse model for syndromic craniosynostosis.Journal of anatomy · 2024Article
- X-linked hypophosphatemia, fibroblast growth factor 23 signaling, and craniosynostosis.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Cranial Neural Crest Specific Deletion ofInternational journal of molecular sciences · 2023Article
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- Development of Erf-Mediated Craniosynostosis and Pharmacological Amelioration.International journal of molecular sciences · 2023Article
- Article
- Synchondrosis fusion contributes to the progression of postnatal craniofacial dysmorphology in syndromic craniosynostosis.Journal of anatomy · 2023Article
- Embryonic and early postnatal cranial bone volume and tissue mineral density values for C57BL/6J laboratory mice.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Mechanical loading of cranial joints minimizes the craniofacial phenotype in Crouzon syndrome.Scientific reports · 2022Article
- Targeting fibroblast growth factor receptors causes severe craniofacial malformations in zebrafish larvae.PeerJ · 2022Article
- Visualization of the Cartilage and Bone Elements in the Craniofacial Structures by Alcian Blue and Alizarin Red Staining.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Deletion of the Pyrophosphate Generating Enzyme ENPP1 Rescues Craniofacial Abnormalities in the TNAPFrontiers in dental medicine · 2022Article
- Gene Therapy Using Adeno-Associated Virus Serotype 8 Encoding TNAP-DJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Characterization of dental pulp stem cells isolated from a patient diagnosed with Crouzon syndrome.Journal of cellular physiology · 2021Article
- Macropore design of tissue engineering scaffolds regulates mesenchymal stem cell differentiation fate.Biomaterials · 2021Article
- Tissue Nonspecific Alkaline Phosphatase Function in Bone and Muscle Progenitor Cells: Control of Mitochondrial Respiration and ATP Production.International journal of molecular sciences · 2021Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Crouzon syndrome is a debilitating congenital disorder involving abnormal craniofacial skeletal development caused by mutations in fibroblast growth factor receptor-2 (FGFR2). Phenotypic expression in humans exhibits an autosomal dominant pattern that commonly involves premature fusion of the coronal suture (craniosynostosis) and severe midface hypoplasia. To further investigate the biologic mechanisms by which the Crouzon syndrome-associated FGFR2(C342Y) mutation leads to abnormal craniofacial skeletal development, we created congenic BALB/c FGFR2(C342Y/+) mice. Here, we show that BALB/c FGFR2(C342Y/+) mice have a consistent craniofacial phenotype including partial fusion of the coronal and lambdoid sutures, intersphenoidal synchondrosis, and multiple facial bones, with minimal fusion of other craniofacial sutures. This phenotype is similar to the classic and less severe form of Crouzon syndrome that involves significant midface hypoplasia with limited craniosynostosis. Linear and morphometric analyses demonstrate that FGFR2(C342Y/+) mice on the BALB/c genetic background differ significantly in form and shape from their wild-type littermates and that in this genetic background the FGFR2(C342Y) mutation preferentially affects some craniofacial bones and sutures over others. Analysis of cranial bone cells indicates that the FGFR2(C342Y) mutation promotes aberrant osteoblast differentiation and increased apoptosis that is more severe in frontal than parietal bone cells. Additionally, FGFR2(C342Y/+) frontal, but not parietal, bones exhibit significantly diminished bone volume and density compared to wild-type mice. These results confirm that FGFR2-associated craniosynostosis occurs in association with diminished cranial bone tissue and may provide a potential biologic explanation for the clinical finding of phenotype consistency that exists between many Crouzon syndrome patients.
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