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JEM:成骨细胞功能调节研究获进展

2013-09-02 黄辛 中国科学报

 近日,《实验医学期刊》在线发表了中科院上海生物化学与细胞生物学研究所研究员邹卫国团队的最新成果。该小组发现,微管结合蛋白DCAMKL1通过抑制转录因子RUNX2活性进而调控成骨细胞的功能。相关研究有望给骨质疏松症患者带来福音。

近日,《实验医学期刊》在线发表了中科院上海生物化学与细胞生物学研究所研究员邹卫国团队的最新成果。该小组发现,微管结合蛋白DCAMKL1通过抑制转录因子RUNX2活性进而调控成骨细胞的功能。相关研究有望给骨质疏松症患者带来福音。【原文阅读】

骨的生长发育和新陈代谢是机体重要的生命活动。成骨细胞来源于中胚层间充质干细胞,能够分泌骨基质并使之发生矿化,从而形成新的骨结构。研究人员通过诱导向成骨细胞分化,并定量检测分化的早期标志物碱性磷酸酶的活性,高通量地筛选出成骨细胞分化的新调节因子。研究发现,微管结合蛋白DCAMKL1被敲低后,间充质干细胞向成骨细胞的分化能力增强。DCAMKL1基因敲除小鼠的成骨细胞功能增强、骨生成速率增加、骨密度增加。

研究表明,DCAMKL1能够通过提高微管蛋白的多聚化,从而抑制成骨细胞分化的主要转录因子RUNX2的活性。RUNX2的多种突变导致人类常染色体显性疾病——锁骨颅骨发育不全(CCD),其特征性表现为锁骨发育不全和持续性颅骨缝开放。

邹卫国表示,该项研究建立了在成骨细胞中运用正向遗传学方法筛选新的调节因子的方法,鉴定了一个调节成骨细胞功能的新的调节因子,提示可能通过调节微管的多聚化来增强骨骼强度,从而治疗骨质疏松症等疾病。

该研究由中科院生物化学与细胞生物学研究所、美国哈佛大学医学院、康奈尔大学、哈佛大学口腔学院、Merck公司的研究人员共同完成,并得到中科院生物化学与细胞生物学研究所启动资金、细胞生物学国家重点实验室资金以及NIH项目的支持。

原文阅读
Zou W, Greenblatt MB, Brady N, Lotinun S, Zhai B, de Rivera H, Singh A, Sun J, Gygi SP, Baron R, Glimcher LH, Jones DC.The microtubule-associated protein DCAMKL1 regulates osteoblast function via repression of Runx2.J Exp Med. 2013 Aug 26;210(9):1793-806. 

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