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Clin Oral Investig. 2014 Jul;18(6):1639-46. doi: 10.1007/s00784-013-1129-6. Epub 2013 Nov 13.

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

Author information

1
Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland, reinhard.gruber@zmk.unibe.ch.

Abstract

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.

PMID:
24221580
DOI:
10.1007/s00784-013-1129-6
[Indexed for MEDLINE]

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