JOURNAL ARTICLE

Bone morphogenetic protein 2 enhances mouse osteoclast differentiation via increased levels of receptor activator of NF-κB ligand expression in osteoblasts

Keita Tachi, Masamichi Takami, Baohong Zhao, Ayako Mochizuki, Atsushi Yamada, Yoichi Miyamoto, Tomio Inoue, Kazuyoshi Baba, Ryutaro Kamijo
Cell and Tissue Research 2010, 342 (2): 213-20
20941510
1α,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] induces osteoclast formation via induction of receptor activator of NF-κB ligand (RANKL, also called TNF-related activation-induced cytokine: TRANCE) in osteoblasts. In cocultures of mouse bone marrow cells and osteoblasts, 1,25(OH)(2)D(3) induced osteoclast formation in a dose-dependent manner, with maximum osteoclast formation observed at concentrations greater than 10(-9) M of 1,25(OH)(2)D(3). In the presence of bone morphogenetic protein 2 (BMP-2), the maximum formation of osteoclasts was seen with lower concentrations of 1,25(OH)(2)D(3) (greater than 10(-11) M), suggesting that BMP-2 enhances osteoclast formation induced by 1,25(OH)(2)D(3). In addition, the expressions of RANKL mRNA and proteins were induced by 1,25(OH)(2)D(3) in osteoblasts, and further upregulated by BMP-2. In mouse bone marrow cell cultures without 1,25(OH)(2)D(3), BMP-2 did not enhance osteoclast differentiation induced by recombinant RANKL and macrophage colony-stimulating factor (M-CSF), indicating that BMP-2 does not target osteoclast precursors. Furthermore, BMP-2 up-regulated the expression level of vitamin D receptor (VDR) in osteoblasts. These results suggest that BMP-2 regulates mouse osteoclast differentiation via upregulation of RANKL in osteoblasts induced by 1,25(OH)(2)D(3).

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