ArticleScientific reports2016
Mutant GDF5 enhances ameloblast differentiation via accelerated BMP2-induced Smad1/5/8 phosphorylation.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 25 citations in OpenAlex.
- FAM20A Deficiency Drives Transcriptomic Dysregulation and Functional Impairment in Gingival Fibroblasts.Cell proliferation · 2026Article
- METTL14 regulates chondrogenesis through the GDF5-RUNX-extracellular matrix gene axis during limb development.Nature communications · 2025Article
- Spatiotemporal Molecular Architecture of Lineage Allocation and Cellular Organization in Tooth Morphogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- G protein-coupled receptorThe Journal of biological chemistry · 2020Article
- Article
- Single-Cell RNA-Sequencing From Mouse Incisor Reveals Dental Epithelial Cell-Type Specific Genes.Frontiers in cell and developmental biology · 2020Article
- Expression Patterns ofFrontiers in cell and developmental biology · 2020Article
- Decreased BMP-7 and p-Smad1/5/8 expression, and increased levels of gremlin in hepatocellular carcinoma.Oncology letters · 2018Article
- TGF-β Family Signaling in Epithelial Differentiation and Epithelial-Mesenchymal Transition.Cold Spring Harbor perspectives in biology · 2018Review
- Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bone morphogenetic proteins (BMPs) regulate hard tissue formation, including bone and tooth. Growth differentiation factor 5 (GDF5), a known BMP, is expressed in cartilage and regulates chondrogenesis, and mutations have been shown to cause osteoarthritis. Notably, GDF5 is also expressed in periodontal ligament tissue; however, its role during tooth development is unclear. Here, we used cell culture and in vivo analyses to determine the role of GDF5 during tooth development. GDF5 and its associated BMP receptors are expressed at the protein and mRNA levels during postnatal tooth development, particularly at a stage associated with enamel formation. Furthermore, whereas BMP2 was observed to induce evidently the differentiation of enamel-forming ameloblasts, excess GDF5 induce mildly this differentiation. A mouse model harbouring a mutation in GDF5 (W408R) showed enhanced enamel formation in both the incisors and molars, but not in the tooth roots. Overexpression of the W408R GDF5 mutant protein was shown to induce BMP2-mediated mRNA expression of enamel matrix proteins and downstream phosphorylation of Smad1/5/8. These results suggest that mutant GDF5 enhances ameloblast differentiation via accelerated BMP2-signalling.
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