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Osteoporotic bone formation in mice lacking tob2 ; involvement of Tob2 in RANK ligand expression and osteoclasts differentiation
Author(s) -
Ajima Rieko,
Akiyama Toru,
Usui Michihiko,
Yoneda Mitsuhiro,
Yoshida Yutaka,
Nakamura Takahisa,
Minowa Osamu,
Noda Masaki,
Tanaka Sakae,
Noda Tetsuo,
Yamamoto Tadashi
Publication year - 2008
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2008.03.012
Subject(s) - calcitriol receptor , rankl , stromal cell , chemistry , endocrinology , medicine , vitamin d and neurology , receptor , rank ligand , bone marrow , osteoclast , microbiology and biotechnology , transcription factor , cancer research , biology , gene , activator (genetics) , biochemistry
Mice lacking tob2 , a member of the antiproliferative family genes, had decreased bone mass, and the number of osteoclasts differentiated from bone marrow cells was increased. Overexpression of Tob2 in stromal cells repressed vitamin D 3 ‐induced osteoclasts formation. Furthermore, expression of RANKL mRNA in stromal cells was increased in the absence of Tob2 and decreased in the presence of Tob2. Tob2 interacted with vitamin D 3 receptor (VDR), which suggests its involvement in vitamin D 3 receptor‐mediated regulation of transcription. Because VDR regulates RANKL expression, our data suggest that Tob2 negatively regulates formation of osteoclasts by suppressing RANKL expression through its interaction with VDR.