ArticlePloS one2014
Therapeutic effect of nanogel-based delivery of soluble FGFR2 with S252W mutation on craniosynostosis.
Article in PloS one, 2014. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Insights and future directions of potential genetic therapy for Apert syndrome: A systematic review.Gene therapy · 2021Pooled it
- Targeted allele-specificMolecular therapy. Nucleic acids · 2025Article
- Unraveling the Complexity of Apert Syndrome: Genetics, Clinical Insights, and Future Frontiers.Cureus · 2023Review
- FGF/FGFR signaling in health and disease.Signal transduction and targeted therapy · 2020Review
- Pharmacological exposures may precipitate craniosynostosis through targeted stem cell depletion.Stem cell research · 2019Article
- Direct Effects of Nicotine Exposure on Murine Calvaria and Calvarial Cells.Scientific reports · 2019Article
- Current Approaches in the Development of Molecular and Pharmacological Therapies in Craniosynostosis Utilizing Animal Models.Molecular syndromology · 2019Review
- Adeno-Associated Virus-Mediated RNAi against Mutant Alleles Attenuates Abnormal Calvarial Phenotypes in an Apert Syndrome Mouse Model.Molecular therapy. Nucleic acids · 2018Article
- Research progress of self-assembled nanogel and hybrid hydrogel systems based on pullulan derivatives.Drug delivery · 2018Review
- Absorbable collagen sponges loaded with recombinant bone morphogenetic protein 9 induces greater osteoblast differentiation when compared to bone morphogenetic protein 2.Clinical and experimental dental research · 2017Article
- Fibroblast Growth Factor Receptor 2 (International journal of biological sciences · 2017Review
- Modeling craniofacial and skeletal congenital birth defects to advance therapies.Human molecular genetics · 2016Review
- A Genetic-Pathophysiological Framework for Craniosynostosis.American journal of human genetics · 2015Review
- Fibroblast growth factor signaling in skeletal development and disease.Genes & development · 2015Review
- Article
- Research advances in Apert syndrome.Journal of oral biology and craniofacial researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apert syndrome is an autosomal dominantly inherited disorder caused by missense mutations in fibroblast growth factor receptor 2 (FGFR2). Surgical procedures are frequently required to reduce morphological and functional defects in patients with Apert syndrome; therefore, the development of noninvasive procedures to treat Apert syndrome is critical. Here we aimed to clarify the etiological mechanisms of craniosynostosis in mouse models of Apert syndrome and verify the effects of purified soluble FGFR2 harboring the S252W mutation (sFGFR2IIIcS252W) on calvarial sutures in Apert syndrome mice in vitro. We observed increased expression of Fgf10, Esrp1, and Fgfr2IIIb, which are indispensable for epidermal development, in coronal sutures in Apert syndrome mice. Purified sFGFR2IIIcS252W exhibited binding affinity for fibroblast growth factor (Fgf) 2 but also formed heterodimers with FGFR2IIIc, FGFR2IIIcS252W, and FGFR2IIIbS252W. Administration of sFGFR2IIIcS252W also inhibited Fgf2-dependent proliferation, phosphorylation of intracellular signaling molecules, and mineralization of FGFR2S252W-overexpressing MC3T3-E1 osteoblasts. sFGFR2IIIcS252W complexed with nanogels maintained the patency of coronal sutures, whereas synostosis was observed where the nanogel without sFGFR2S252W was applied. Thus, based on our current data, we suggest that increased Fgf10 and Fgfr2IIIb expression may induce the onset of craniosynostosis in patients with Apert syndrome and that the appropriate delivery of purified sFGFR2IIIcS252W could be effective for treating this 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.