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PMID:23116709
| Citation |
'Kim, TH, Lee, B, Kwon, E, Choi, CH, Sung, IH, Kim, Y, Sohn, J and Ji, JD (2012) 1,25-dihydroxyvitamin D(3) inhibits directly human osteoclastogenesis by down-regulation of the c-Fms and RANK expression. Joint Bone Spine ' |
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| Abstract |
OBJECTIVE: 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) is a key molecule to maintain calcium homeostasis and bone metabolism. It was recently reported that 1,25(OH)(2)D(3) directly inhibited osteoclast differentiation in mouse bone marrow cells and human bone marrow-derived colony-forming unit granulocyte macrophage (CFU-GM) cells. However, the direct effects of 1,25(OH)(2)D(3) and its affecting mechanisms on the osteoclast differentiation of human osteoclast precursors remain largely unknown. In this study, we examined the direct effects of 1,25(OH)(2)D(3) on the osteoclastogenesis of human peripheral blood (PB) osteoclast precursors. METHODS: In vitro osteoclastogenesis assays were performed using osteoclast precursors from normal PB. The gene expressions were analyzed using real-time PCR. The cell surface proteins, including c-Fms and RANK, were measured by flow cytometry. RESULTS: 1,25(OH)(2)D(3) strongly inhibited osteoclast differentiation and it suppressed the expression of RANK in the human PB osteoclast precursors. One mechanism of RANK inhibition by 1,25(OH)(2)D(3) is down-regulation of the M-CSF receptor c-Fms, which is required for the expression of RANK. In contrast to the previous reports on mouse osteoclast precursors, 1,25(OH)(2)D(3) did not affect the expression of c-Fos. Parallel to the inhibition of osteoclastogenesis, 1,25(OH)(2)D(3) increased the expression and phosphorylation of CCAAT enhancer-binding protein β (C/EBPβ), which is a recently discovered inhibitor of osteoclastogenesis. CONCLUSIONS: Our results show that 1,25(OH)(2)D(3) inhibits human osteoclastogenesis by decreasing the RANK+ osteoclast precursors, and we suggest that 1,25(OH)(2)D(3) may be a powerful therapeutic agent for treating inflammation-induced bone disease that shows excessive osteoclast activation. |
| Links |
PubMed Online version:10.1016/j.jbspin.2012.09.011 |
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