Erk pathways negatively regulate matrix mineralization
Erk pathways negatively regulate matrix mineralization
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DOI：
10.1016/j.bone.2006.07.024
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发表时间：
2007-01-01
期刊：
影响因子：
4.1
通讯作者：
Tanaka, Sakae
中科院分区：
文献类型：
--
作者：
Kono, Shin-jiro;Oshima, Yasushi;Tanaka, Sakae
骨矿化是调节钙化组织力学性能的重要步骤，但矿化背后的分子事件仍然难以捉摸。我们研究了细胞外信号调节激酶（Erk）途径在体外和体内成骨细胞基质矿化中的作用。PD98059 Mek抑制剂处理或腺病毒载体介导的显性负Ras（Ras(DN)）表达增加了成骨前细胞MLO-A5细胞和成骨细胞MC3T3-E1细胞的基质矿化，并被血小板衍生生长因子（PDGF）处理或组成型活性Mek I （Mek(CA)）表达激活的Erk抑制。携带Ras（DN）基因的腺病毒载体对1日龄小鼠颅部矿化作用增强，而Mek CA腺病毒载体对颅部矿化作用抑制。这些结果表明，Erk通路是体外和体内基质矿化的负调节因子。(c) 2006年爱思唯尔公司。版权所有。
Skeletal mineralization is an important step regulating the mechanical properties of the calcified tissues, but molecular events underlying mineralization still remain elusive. We examined the role of extracellular signal-regulated kinase (Erk) pathways in matrix mineralization of osteogenic cells both in vitro and in vivo. Matrix mineralization by preosteocytic MLO-A5 cells and osteoblastic MC3T3-E1 cells was increased by either PD98059 Mek inhibitor treatment or adenovirus vector-mediated dominant negative Ras (Ras(DN)) expression and was suppressed by Erk activation by platelet-derived growth factor (PDGF) treatment or constitutively active Mek I (Mek(CA)) expression. Administration of adenovirus vectors carrying Ras(DN) gene onto the calvaria of 1-day-old mice increased the mineralization of the tissues, while that of the Mek CA adenovirus suppressed it. These results suggest that the Erk pathway is a negative regulator of the matrix mineralization both in vitro and in vivo. (c) 2006 Elsevier lnc. All rights reserved.