Runx2 determines bone maturity and turnover rate in postnatal bone loss in estrogen deficiency
Runx2 determines bone maturity and turnover rate in postnatal bone loss in estrogen deficiency
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DOI：
10.1002/dvdy.21187
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发表时间：
2007-07-01
影响因子：
2.5
通讯作者：
Komori, Toshihisa
中科院分区：
文献类型：
--
作者：
Maruyama, Zenjiro;Yoshida, Carolina A.;Komori, Toshihisa
Runx 2是成骨细胞分化的重要转录因子。然而，Runx 2在出生后骨发育中的功能仍有待阐明。引入显性阴性（dn）-Runx 2没有抑制成熟成骨细胞中Col 1a 1和骨钙素的表达。在成骨细胞中表达dn-Runx 2的转基因小鼠中，松质骨的矿化增加，体积增加，具有密质骨的特征，并且主要骨基质蛋白基因的表达相对维持。卵巢切除后，骨溶解和骨形成均未增强，骨相对保存。在野生型小鼠中，Runx 2在未成熟的成骨细胞中强烈表达，但在成骨细胞成熟过程中下调。这些发现表明，骨的成熟度和周转率是由功能性Runx 2的水平和Runx 2是负责雌激素缺乏时的骨丢失，但Runx 2是不必要的主要骨基质蛋白基因的表达，在出生后的骨发育和维护的维护。发展动力学236：1876-1890，2007年。(c)2007 Wiley-Liss，Inc.
Runx2 is an essential transcription factor for osteoblast differentiation. However, the functions of Runx2 in postnatal bone development remain to be clarified. Introduction of dominant-negative (dn)-Runx2 did not inhibit Col1a1 and osteocalcin expression in mature osteoblastic cells. In transgenie mice that expressed dn-Runx2 in osteoblasts, the trabecular bone had increased mineralization, increased volume, and features of compact bone, and the expression of major bone matrix protein genes was relatively maintained. After ovariectomy, neither osteolysis nor bone formation was enhanced and bone was relatively conserved. In wild-type mice, Runx2 was strongly expressed in immature osteoblasts but downregulated during osteoblast maturation. These findings indicate that the maturity and turnover rate of bone are determined by the level of functional Runx2 and Runx2 is responsible for bone loss in estrogen deficiency, but that Runx2 is not essential for maintenance of the expression of major bone matrix protein genes in postnatal bone development and maintenance. Developmental Dynamics 236:1876-1890, 2007. (c) 2007 Wiley-Liss, Inc.