Amelogenin is a negative regulator of osteoclastogenesis via downregulation of RANKL, M-CSF and fibronectin expression in osteoblasts
Amelogenin is a negative regulator of osteoclastogenesis via downregulation of RANKL, M-CSF and fibronectin expression in osteoblasts
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DOI：
10.1016/j.archoralbio.2006.09.016
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发表时间：
2007-03-01
影响因子：
3
通讯作者：
Fukumoto, Satoshi
中科院分区：
文献类型：
--
作者：
Nishiguchi, Miyuki;Yuasa, Kenji;Fukumoto, Satoshi
釉原蛋白是一种新的釉基质蛋白。基因敲除小鼠表现出破骨细胞形成和牙骨质吸收增强。本研究探讨釉原蛋白对破骨细胞生成的影响。在与颅骨成骨细胞和纯化的骨髓细胞共培养中，釉原蛋白显着抑制破骨细胞的生成。此外，釉原蛋白抑制成骨细胞核因子KB配体受体激活剂（RANKL）、巨噬细胞集落刺激因子（M-CSF）和纤连蛋白的表达，而RANKL的表达受到纤连蛋白的诱导，并被纤连蛋白小干扰RNA抑制。这些结果表明，釉原蛋白对破骨细胞生成的抑制作用导致成骨细胞中RANKL、M-CSF和纤连蛋白的产生下调。(c)2006爱思唯尔有限公司版权所有
Amelogenin is a novel enamel matrix protein. Knockout mice showed enhanced osteoclast formation and resorption of tooth cementum. This study investigated the effects of amelogenin on osteoclastogenesis. In co-cultures with calvaria osteoblasts and purified bone marrow cells, amelogenin inhibited osteoclastogenesis dramatically. Furthermore, amelogenin inhibited the expression of receptor activator of nuclear factor KB ligand (RANKL), macrophage-colony stimulating factor (M-CSF) and fibronectin in osteoblasts, while RANKL expression was induced by fibronectin and inhibited by treatment with fibronectin small interfering RNA. These results suggest that the inhibitory effects of amelogenin on osteoclastogenesis lead to downregulation of RANKL, M-CSF and fibronectin production in osteoblasts. (c) 2006 Elsevier Ltd. All rights reserved