Inductive effects of dexamethasone on the mineralization and the osteoblastic gene expressions in mature osteoblast-like ROS17/2.8 cells

Inductive effects of dexamethasone on the mineralization and the osteoblastic gene expressions in mature osteoblast-like ROS17/2.8 cells
复制标题

DOI:
10.1016/j.bbrc.2007.07.192
复制
发表时间:
2007-10-19
影响因子:
3.1
通讯作者:
Takagi, Minoru
Takagi, Minoru
中科院分区:
生物学4区
文献类型:
--
作者:
Mikami, Yoshikazu;Omoteyama, Kazuki;Takagi, Minoru

文献摘要

被引文献

相似文献

我们研究了地塞米松(Dex),一种合成的糖皮质激素,对矿化骨结节的形成和晚期成骨细胞标志物,骨涎蛋白(BSP),骨钙素(OC),骨桥蛋白(OPN)在成熟成骨细胞ROS 17/2.8细胞中的基因表达的影响。用Dex处理ROS 17/2.8细胞导致矿化诱导,伴随BSP和OC表达增加。以前的研究表明BSP和OC的表达受Runx 2的调控。然后,我们假设Dex可能通过Runx 2促进ROS 17/2.8上的成骨细胞分化和矿化。在这项研究中,没有观察到Runx 2的mRNA和蛋白表达的影响。然而,Runx 2的转录活性被Dex处理增强。转染Runx 2小干扰RNA(siRNA)后,Dex诱导的BSP和OC表达降低。这些结果表明,通过Dex处理增强Runx 2转录活性可能随后激活成骨细胞标记基因,如BSP和OC,从而产生随后矿化的骨特异性基质。(C)2007爱思唯尔公司All rights reserved.
We examined the effects of dexamethasone (Dex), a synthetic glucocorticoid, on the formation of mineralized bone nodules and the gene expressions of the late ostcoblastic markers, bone sialoprotein (BSP), osteocalcin (OC), and osteopontin (OPN) in mature osteoblast ROS17/2.8 cells. Treatment of ROS17/2.8 cells with Dex resulted in the induction of mineralization accompanied with increasing BSP and OC expressions. Previous reports have demonstrated that BSP and OC expressions are regulated by Runx2. Then, we hypothesized that Dex might promote osteoblastic differentiation and mineralization on ROS 17/2.8 by Runx2. In this study, no effect was observed in mRNA and protein expression of Runx2. However, the transcriptional activity of Runx2 was enhanced by Dex treatment. Furthermore, the Dex-induced BSP and OC expressions decreased after the transfection of Runx2 small-interfering RNAs (siRNAs). These results suggested that the enhancement of Runx2 transcriptional activity by Dex treatment may be followed by the activation of ostcoblast marker genes, such as BSP and OC to thereby produce a bone-specific matrix that subsequently becomes mineralized. (C) 2007 Elsevier Inc. All rights reserved.