ArticleClinical oral investigations2014
TGF-βRI kinase activity mediates Emdogain-stimulated in vitro osteoclastogenesis.
Article in Clinical oral investigations, 2014. 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, 22 citations in OpenAlex.
- RNAseq of peripheral blood mononucleated cells exposed to platelet-rich fibrin and enamel matrix derivatives.Scientific reports · 2025Article
- The role of enamel matrix derivatives in periodontal regeneration following tooth replantation/transplantation: a narrative review of post-reperfusion injury.Frontiers in cell and developmental biology · 2025Review
- Enamel Matrix Derivative Suppresses Chemokine Expression in Oral Epithelial Cells.International journal of molecular sciences · 2023Article
- TGF-β Signalling Mediates the Anti-Inflammatory Activity of Enamel Matrix Derivative In Vitro.International journal of molecular sciences · 2022Article
- The role of menin in bone pathology.Endocrine connections · 2022Review
- Article
- Effect of Enamel Matrix Derivatives on Osteoclast Formation from PBMC of Periodontitis Patients and Healthy Individuals after Interaction with Activated Endothelial Cells.Medicina (Kaunas, Lithuania) · 2021Article
- Glucagon-like peptide 2 decreases osteoclasts by stimulating apoptosis dependent on nitric oxide synthase.Cell proliferation · 2018Article
- Enamel matrix proteins exhibit growth factor activity: A review of evidence at the cellular and molecular levels.Experimental and therapeutic medicine · 2015Article
- Emdogain-regulated gene expression in palatal fibroblasts requires TGF-βRI kinase signaling.PloS one · 2014Article
- Novel biological activity of ameloblastin in enamel matrix derivative.Journal of applied oral science : revista FOBArticle
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesEmdogain, containing an extract of fetal porcine enamel matrix proteins, is a potent stimulator of in vitro osteoclastogenesis. The underlying molecular mechanisms are, however, unclear. MATERIAL AND
methodsHere, we have addressed the role of transforming growth factor-beta receptor type 1 (TGF-βRI) kinase activity on osteoclastogenesis in murine bone marrow cultures.
resultsInhibition of TGF-βRI kinase activity with SB431542 abolished the effect of Emdogain on osteoclastogenesis induced by receptor activator of nuclear factor kappa-B ligand or tumor necrosis factor-alpha. SB431542 also suppressed the Emdogain-mediated increase of OSCAR, a co-stimulatory protein, and dendritic cell-specific transmembrane protein and Atp6v0d2, the latter two being involved in cell fusion. Similar to transforming growth factor-beta1 (TGF-β), Emdogain could not compensate for the inhibition of IL-4 and IFNγ on osteoclast formation. When using the murine macrophage cell line RAW246.7, SB431542 and the smad-3 inhibitor SIS3 blocked Emdogain-stimulated expression of the transcription factor NFATc1.
conclusionsTaken together, the data suggest that TGF-βRI kinase activity is necessary to mediate in vitro effects of Emdogain on osteoclastogenesis. CLINICAL RELEVANCE: Based on these in vitro data, we can speculate that at least part of the clinical effects of Emdogain on osteoclastogenesis is mediated via TGF-β signaling.
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