TGF-beta enhances osteoclast differentiation in hematopoietic cell cultures stimulated with RANKL and M-CSF.

Autor: Sells Galvin RJ; Lilly Research Labs, Lilly Corporate Center, Indianapolis, Indiana, 46285, USA. Galvin_Rachelle_J_S@Lilly.com, Gatlin CL, Horn JW, Fuson TR
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 1999 Nov; Vol. 265 (1), pp. 233-9.
DOI: 10.1006/bbrc.1999.1632
Abstrakt: TGF-beta has been shown to inhibit and stimulate osteoclastogenesis. The purpose of this study was to evaluate the effects of TGF-beta in hematopoietic cell cultures stimulated with RANKL and M-CSF. In cocultures of hematopoietic cells and BALC cells (a calvarial-derived cell line), TGF-beta inhibited tartrate-resistant acid phosphatase (TRAP)-positive multinucleated cell formation. In contrast, TGF-beta enhanced TRAP-positive multinucleated cell formation up to 10-fold in hematopoietic cell cultures containing few osteoblastic/stromal cells. Likewise, TGF-beta increased the number of calcitonin receptor (CTR)-positive multinucleated and mononucleated cells in a concentration-dependent manner. An increase in cell size and multinuclearity was also observed in the presence of TGF-beta. The stimulatory effects of TGF-beta were dependent on the presence of M-CSF and RANKL. When differentiated on bovine cortical bone slices, these cells formed resorption lacunae. These results suggest that TGF-beta has a direct stimulatory effect on osteoclastogenesis in hematopoietic cells treated with RANKL and M-CSF.
(Copyright 1999 Academic Press.)
Databáze: MEDLINE
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