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B Ligand and Macrophage-Colony- Stimulating Factor1
*
Department of Oral Anatomy, Meikai University School of Dentistry, Sakado, Saitama, Japan; and
Department of Bioscience, Faculty of Applied Bioscience, Tokyo University of Agriculture, Setagaya, Tokyo, Japan
Differentiation of osteoclasts, the cells primarily responsible for
bone resorption, is controlled by a variety of osteotropic hormones and
cytokines. Of these factors, receptor activator of NF-
B (RANK)
ligand (RANKL) has been recently cloned as an essential inducer of
osteoclastogenesis in the presence of M-CSF. Here, we isolated a
stroma-free population of monocyte/macrophage (M/M
)-like hemopoietic
cells from mouse unfractionated bone cells that were capable of
differentiating into mature osteoclasts by treatment with soluble RANKL
(sRANKL) and M-CSF. However, the efficiency of osteoclast formation was
low, suggesting the requirement for additional factors. The isolated
M/M-like hemopoietic cells expressed TGF-ß and type I and II
receptors of TGF-ß. Therefore, we examined the effect of TGF-ß on
osteoclastogenesis. TGF-ß with a combination of sRANKL and M-CSF
promoted the differentiation of nearly all M/M-like hemopoietic
cells into cells of the osteoclast lineage. Neutralizing
anti-TGF-ß Ab abrogated the osteoclast generation. These TGF-ß
effects were also observed in cultures of unfractionated bone cells,
and anti-TGF-ß blocked the stimulatory effect of
1,25-dihydroxyvitamin D3. Translocation of NF-B into
nuclei induced by sRANKL in TGF-ß-pretreated M/M-like hemopoietic
cells was greater than that in untreated cells, whereas TGF-ß did not
up-regulate the expression of RANK, the receptor of RANKL. Our findings
suggest that TGF-ß is an essential autocrine factor for
osteoclastogenesis.
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