Enhancement of osteoblast differentiation that is inhibited by titanium particles through inactivation of NFATc1 by VIVIT peptide

Enhancement of osteoblast differentiation that is inhibited by titanium particles through inactivation of NFATc1 by VIVIT peptide
复制标题

通过 VIVIT 肽灭活 NFATc1,增强钛颗粒抑制的成骨细胞分化。

DOI:
10.1002/jbm.a.32891
复制
发表时间:
2010-12-01
影响因子:
4.9
通讯作者:
Tang Tingting
Tang Tingting
中科院分区:
工程技术3区
文献类型:
--
作者:
Li Maoqiang;Zhu Zhenan;Tang Tingting

文献摘要

被引文献

相似文献

骨形成受到颗粒状磨损碎屑的抑制,是导致假体周围骨质溶解的病理因素。尽管已知活化T细胞核因子c1(NFATc 1)参与成骨细胞分化,但其对成骨细胞响应磨损颗粒的作用仍不清楚。在这项研究中,我们研究了NFATc 1在调节成骨细胞分化的大鼠颅骨(RC)细胞(细胞培养模型,包括许多骨祖细胞),钛(Ti)颗粒的挑战的作用。结果表明,钛颗粒抑制RC细胞的成骨分化和矿化。NFATc 1在钛颗粒抑制RC细胞向成骨细胞分化的过程中起关键作用。通过11 R-VIVIT肽灭活NFATc 1可有效增强钛颗粒对成骨细胞分化和矿化的抑制作用。11 R-VIVIT肽对RC细胞没有毒性作用。基于这些数据,我们得出结论,11 R-VIVIT肽对NFATc 1的灭活可能为通过增加骨形成治疗假体周围骨溶解提供了一个有前途的治疗靶点。(C)2010 Wiley Periodicals,Inc. J Biomed Mater Res Part A:95A:727-734,2010.
Bone formation, which is inhibited by particulate wear debris, is a pathological factor that contributes to periprosthetic osteolysis. Although the nuclear factor of activated T cells c1 (NFATc1) is known to be involved in osteoblast differentiation, and its effect on osteoblasts in response to wear particles remains unclear. In this study, we investigated the role of NFATc1 in the regulation of osteoblastic differentiation of rat calvaria (RC) cells (a cell-culture model comprising many osteoprogenitors) that were challenged with titanium (Ti) particles. The results showed that the Ti particles inhibited osteoblastic differentiation and mineralization of RC cells. NFATc1 plays a critical role in the Ti-particle inhibition process of the osteoblastic differentiation in RC cells. Inactivation of NFATc1 by the 11R-VIVIT peptide potently enhanced osteoblast differentiation and mineralization inhibition by the Ti particles. The 11R-VIVIT peptide does not have a toxic effect on the RC cells. On the basis of these data, we conclude that inactivation of NFATc1 by the 11R-VIVIT peptide may provide a promising therapeutic target for the treatment of periprosthetic osteolysis by increasing bone formation. (C) 2010 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 95A: 727-734, 2010.