Trial reportThe American journal of pathology1999
Decreased proliferation and altered differentiation in osteoblasts from genetically and clinically distinct craniosynostotic disorders.
Trial report in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 90 citations in OpenAlex.
- Erf Affects Commitment and Differentiation of Osteoprogenitor Cells in Cranial Sutures via the Retinoic Acid Pathway.Molecular and cellular biology · 2021Article
- Characterization of dental pulp stem cells isolated from a patient diagnosed with Crouzon syndrome.Journal of cellular physiology · 2021Article
- Metformin Promotes Neuronal Differentiation via Crosstalk between Cdk5 and Sox6 in Neuroblastoma Cells.Evidence-based complementary and alternative medicine : eCAM · 2019Article
- iTRAQ-Based Proteomic Analysis reveals possible target-related proteins and signal networks in human osteoblasts overexpressing FGFR2.Proteome science · 2018Article
- Understanding craniosynostosis as a growth disorder.Wiley interdisciplinary reviews. Developmental biology · 2016Review
- Article
- Inhibited Wnt signaling causes age-dependent abnormalities in the bone matrix mineralization in the Apert syndrome FGFR2(S252W/+) mice.PloS one · 2015Article
- Analysis of human alveolar osteoblast behavior on a nano-hydroxyapatite substrate: an in vitro study.BMC oral health · 2014Article
- Therapeutic effect of nanogel-based delivery of soluble FGFR2 with S252W mutation on craniosynostosis.PloS one · 2014Article
- The molecular and cellular basis of Apert syndrome.Intractable & rare diseases research · 2013Review
- Further analysis of the Crouzon mouse: effects of the FGFR2(C342Y) mutation are cranial bone-dependent.Calcified tissue international · 2013Article
- Postnatal brain and skull growth in an Apert syndrome mouse model.American journal of medical genetics. Part A · 2013Article
- Craniosynostosis-associated Fgfr2(C342Y) mutant bone marrow stromal cells exhibit cell autonomous abnormalities in osteoblast differentiation and bone formation.BioMed research international · 2013Article
- Novel pHEMA-gelatin SPHs as bone scaffolds in dynamic cultures.Journal of materials science. Materials in medicine · 2012Article
- Gene expression profiling in human craniosynostoses: a tool to investigate the molecular basis of suture ossification.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2012Review
- Investigation of FGFR2-IIIC signaling via FGF-2 ligand for advancing GCT stromal cell differentiation.PloS one · 2012Article
- Differential growth factor adsorption to calvarial osteoblast-secreted extracellular matrices instructs osteoblastic behavior.PloS one · 2011Article
- Activation of p38 MAPK pathway in the skull abnormalities of Apert syndrome Fgfr2(+P253R) mice.BMC developmental biology · 2010Article
- Interaction between the glucocorticoid and erythropoietin receptors in human erythroid cells.Experimental hematology · 2009Article
- Craniosynostosis Secondary to Rickets: Manifestations on Computed Tomography.Radiology case reports · 2007Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Craniosynostoses are a heterogeneous group of disorders characterized by premature fusion of cranial sutures. Mutations in fibroblast growth factor receptors (FGFRs) have been associated with a number of such conditions. Nevertheless, the cellular mechanism(s) involved remain unknown. We analyzed cell proliferation and differentiation in osteoblasts obtained from patients with three genetically and clinically distinct craniosynostoses: Pfeiffer syndrome carrying the FGFR2 C342R substitution, Apert syndrome with FGFR2 P253R change, and a nonsyndromic craniosynostosis without FGFR canonic mutations, as compared with control osteoblasts. Osteoblasts from craniosynostotic patients exhibited a lower proliferation rate than control osteoblasts. P253R and nonsyndromic craniosynostosis osteoblasts showed a marked differentiated phenotype, characterized by high alkaline phosphatase activity, increased mineralization and expression of noncollagenous matrix proteins, associated with high expression and activation of protein kinase Calpha and protein kinase Cepsilon isoenzymes. By contrast, the low proliferation rate of C342R osteoblasts was not associated with a differentiated phenotype. Although they showed higher alkaline phosphatase activity than control, C342R osteoblasts failed to mineralize and expressed low levels of osteopontin and osteonectin and high protein kinase Czeta levels. Stimulation of proliferation and inhibition of differentiation were observed in all cultures on FGF2 treatment. Our results suggest that an anticipated proliferative/differentiative switch, associated with alterations of the FGFR transduction pathways, could be the causative common feature in craniosynostosis and that mutations in distinct FGFR2 domains are associated with an in vitro heterogeneous differentiative phenotype.
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