ArticleJournal of cellular and molecular medicine2019
Mutant hFGF23(A12D) stimulates osteoblast differentiation through FGFR3.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 9 citations in OpenAlex.
- Genetic factors underlying Mandibular prognathism: insights from recent human and animal studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Review
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Mir24-2-5p suppresses the osteogenic differentiation with Gnai3 inhibition presenting a direct target via inactivating JNK-p38 MAPK signaling axis.International journal of biological sciences · 2021Article
- Mutant hFGF23(A12D) stimulates osteoblast differentiation through FGFR3.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor (FGF) 23 is a member of the FGF family involved in bone development by interacting with FGFRs. In a previous study, we discovered a mutant human FGF (hFGF) 23 (A12D) in the mandibular prognathism (MP) pedigree. However, the exact role of hFGF23(A12D) during bone formation remains unclear. The aim of this study was to identify the function of hFGF23(A12D) in bone formation. We infected isolated rat calvaria (RC) cells with the recombinant lentivirus containing mutant hFGF23(A12D) and WT hFGF23 respectively. Real-time PCR, western blot and enzyme-linked immunosorbent assay confirmed that hFGF23(A12D) failed to be secreted. We measured cell growth via the CCK-8 assay based on Zsgreen expression, detected cell differentiation ability via alkaline phosphatase staining, performed RT-PCR and found that hFGF23(A12D) inhibited proliferation of RC cells and stimulated the differentiation of RC cells to osteoblasts. Through RNA sequencing, RT-PCR and western blot, we found increased expression of FGFR3. Through co-immunoprecipitation assays and immunofluorescence staining, we revealed that hFGF23(A12D) activated the mitogen-activated protein kinase signalling pathway through interactions with the intracellular domain of FGFR3. In summary, we determined the mechanisms of hFGF23(A12D) involved in osteoblast generation and formation which is specifically due to its interaction with FGFR3.
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