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TGF-βRI kinase activity mediates Emdogain-stimulated in vitro osteoclastogenesis

Gruber, Reinhard ; Roos, Gilles ; Caballé-Serrano, Jordi ; Miron, Rick ; Bosshardt, Dieter ; Sculean, Anton

In: Clinical Oral Investigations, 2014, vol. 18, no. 6, p. 1639-1646

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    Titel
    • TGF-βRI kinase activity mediates Emdogain-stimulated in vitro osteoclastogenesis
    Autor
    • Gruber, Reinhard. Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Roos, Gilles. Laboratory of Oral Cell Biology, School of Dental Medicine, University of Bern, Freiburgstrasse 7, 3010, Bern, Switzerland
    • Caballé-Serrano, Jordi. Department of Oral Surgery and Stomatology, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Miron, Rick. Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Bosshardt, Dieter. Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Sculean, Anton. Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
    Dokumententyp
    • Postprint
    Sprache
    • Englisch
    Veröffentlicht in
    • Clinical Oral Investigations, 2014, vol. 18, no. 6, p. 1639-1646. Springer Berlin Heidelberg
    Andere elektronische Ausgabe
    OAI-PMH-ID
    • oai:doc.rero.ch:325215
    Summary
    Objectives: Emdogain, 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 methods: Here, we have addressed the role of transforming growth factor-beta receptor type 1 (TGF-βRI) kinase activity on osteoclastogenesis in murine bone marrow cultures. Results: Inhibition 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. Conclusions: Taken 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.