Osteoporotic bone formation in mice lacking tob2;: involvement of Tob2 in RANK ligand expression and osteoclasts differentiation
Osteoporotic bone formation in mice lacking tob2;: involvement of Tob2 in RANK ligand expression and osteoclasts differentiation
复制标题
DOI：
10.1016/j.febslet.2008.03.012
复制
发表时间：
2008-04-16
期刊：
影响因子：
3.5
通讯作者：
Yamamoto, Tadashi
中科院分区：
文献类型：
--
作者：
Ajima, Rieko;Akiyama, Toru;Yamamoto, Tadashi
缺乏抗增殖基因家族成员之一的小鼠骨量减少，骨髓细胞分化的破骨细胞数量增加。Tob 2在基质细胞中的过表达抑制维生素D-3诱导的破骨细胞形成。此外，基质细胞中RANKL mRNA的表达在不存在Tob 2的情况下增加，在存在Tob 2的情况下减少。Tob 2与维生素D-3受体（VDR）相互作用，这表明其参与维生素D-3受体介导的转录调节。由于VDR调节RANKL表达，我们的数据表明Tob 2通过与VDR相互作用抑制RANKL表达，从而负调节破骨细胞的形成。(c)2008年欧洲生物化学学会联合会。由Elsevier B出版。版权所有© 2016
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. (c) 2008 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.