Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor osteoprotegerin
Severe osteoporosis in mice lacking osteoclastogenesis inhibitory factor osteoprotegerin
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DOI：
10.1006/bbrc.1998.8697
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发表时间：
1998-06-29
影响因子：
3.1
通讯作者：
Ozawa, H
中科院分区：
文献类型：
--
作者：
Mizuno, A;Amizuka, N;Ozawa, H
破骨细胞是吸收骨的多核细胞。破骨细胞生成抑制因子（OCIF），又称骨保护素（OPG），是破骨细胞分化因子的一种天然诱饵受体，介导破骨细胞祖细胞向破骨细胞分化的重要信号。在这里，我们表明，OCIF/OPG基因敲除小鼠表现出严重的骨质疏松症，由于增强破骨细胞生成时，他们成长为成年人。这些小鼠是可存活和可繁殖的。他们表现出显着的骨丢失伴随着破坏生长板和缺乏骨小梁在他们的股骨。他们的骨骼强度急剧下降。这些结果表明，OCIF/OPG是一个关键因素，作为一个负调节剂，对破骨细胞生成。OCIF/OPG基因敲除小鼠提供了第一个无其他明显异常的骨质疏松症动物模型。(C)北京：科学出版社.
Osteoclasts are multinucleated cells that resorb bone. Osteoclastogenesis inhibitory factor (OCIF), also called osteoprotegerin (OPG), acts as a naturally occurring decoy receptor for osteoclast differentiation factor, which mediates an essential signal to osteoclast progenitors for their differentiation into osteoclasts. Here we show that the OCIF/OPG knockout mice exhibited severe osteoporosis due to enhanced osteoclastogenesis when they grew to be adults. These mice were viable and fertile. They exhibited marked bone loss accompanied by destruction of growth plate and lack of trabecular bone in their femurs. The strength of their bones dramatically decreased. These results demonstrate that OCIF/OPG; is a key factor acting as a negative regulator against osteoclastogenesis. The OCIF/OPG knockout mice provide the first animal model for osteoporosis without other obvious abnormalities. (C) 1998 Academic Press.