ArticlePloS one2021
Fibroblast Growth Factor 9 (FGF9) negatively regulates the early stage of chondrogenic differentiation.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- FGF9 attenuates osteoarthritis progression through the NRF2/GPX3 antioxidant axis.Bone & joint research · 2026Article
- Vitamin A Supplementation Induces AMFK Production to Promote Cartilage Proliferation and Antler Growth in Sika Deer.Animals : an open access journal from MDPI · 2025Article
- FGF9 treatment reduces off-target chondrocytes from iPSC-derived kidney organoids.NPJ Regenerative medicine · 2025Article
- Bupivacaine Reduces the Viability of SH-SY5Y Cells and Promotes Apoptosis by the Inhibition of Akt Signaling Pathway.Neurochemical research · 2025Article
- Fibroblast Growth Factor 19 Disrupts Cartilage Development Via the FGFR4/β-catenin Axis.International journal of biological sciences · 2025Article
- Chromatin profiling and state predictions reveal insights into epigenetic regulation during early porcine development.Epigenetics & chromatin · 2024Article
- Article
- FGF9 Promotes Expression of HAS2 in Palatal Elevation via the Wnt/β-Catenin/TCF7L2 Pathway.Biomolecules · 2022Article
- Whole-genome resequencing reveals molecular imprints of anthropogenic and natural selection in wild and domesticated sheep.Zoological research · 2022Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Limb Mesoderm and Head Ectomesenchyme Both Express a Core Transcriptional Program During Chondrocyte Differentiation.Frontiers in cell and developmental biology · 2022Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibroblast growth factor signaling is essential for mammalian bone morphogenesis and growth, involving membranous ossification and endochondral ossification. FGF9 has been shown to be an important regulator of endochondral ossification; however, its role in the early differentiation of chondrocytes remains unknown. Therefore, in this study, we aimed to determine the role of FGF9 in the early differentiation of chondrogenesis. We found an increase in FGF9 expression during proliferating chondrocyte hypertrophy in the mouse growth plate. Silencing of FGF9 promotes the growth of ATDC5 cells and promotes insulin-induced differentiation of ATDC5 chondrocytes, which is due to increased cartilage matrix formation and type II collagen (col2a1) and X (col10a1), Acan, Ihh, Mmp13 gene expression. Then, we evaluated the effects of AKT, GSK-3β, and mTOR. Inhibition of FGF9 significantly inhibits phosphorylation of AKT and GSK-3β, but does not affected the activation of mTOR. Furthermore, phosphorylation of inhibited AKT and GSK-3β was compensated using the AKT activator SC79, and differentiation of ATDC5 cells was inhibited. In conclusion, our results indicate that FGF9 acts as an important regulator of early chondrogenesis partly through the AKT/GSK-3β pathway.
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