Nuclear Factor I-C promotes proliferation and differentiation of apical papilla-derived human stem cells in vitro

被引:34
作者
Zhang, Jing [1 ,2 ]
Wang, Zhihua [1 ]
Jiang, Yong [1 ]
Niu, Zhongying [3 ]
Fu, Lei [1 ]
Luo, Zhirong [1 ]
Cooper, Paul R. [4 ]
Smith, Anthony J. [4 ]
He, Wenxi [1 ]
机构
[1] Fourth Mil Med Univ, Sch Stomatol, Dept Operat Dent & Endodont, State Key Lab Mil Stomatol, Xian 710032, Peoples R China
[2] Anhui Med Univ, Key Lab Oral Dis Res Anhui Prov, Stomatol Hosp & Coll, Hefei, Peoples R China
[3] 306th Hosp Peoples Liberat Army, Treatment Ctr oral Dis, Beijing, Peoples R China
[4] Univ Birmingham, Sch Dent, Oral Biol, Birmingham B4 6NN, W Midlands, England
基金
中国国家自然科学基金;
关键词
SCAPs; Nuclear factor; Proliferation; Differentiation; TOOTH ROOT DEVELOPMENT; ODONTOBLAST DIFFERENTIATION; DENTAL-PULP; GENE; TRANSCRIPTION; REGENERATION; DISRUPTION; BONE;
D O I
10.1016/j.yexcr.2015.01.020
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
The transcription factor Nuclear Factor I-C (NFIC) has been implicated in the regulation of tooth root development, where it may be anticipated to impact on the behavior of stem cells from the apical papilla (SCAPs) and root odontoblast activity. We hypothesized that NFIC may provide an important target for promoting dentin/root regeneration. In the present study, the effects of NFIC on the proliferation and differentiation of SCAPs were investigated. Over-expression of NFIC increased cell proliferation, mineralization nodule formation and alkaline phosphatase (ALP) activity in SCAPs. Furthermore, NFIC up-regulated the mRNA levels of odontogenic-related markers, ALP, osteocalcin and collagen type I as well as dentin sialoprotein protein levels. In contrast, knockdown of NFIC by si-RNA inhibited the mineralization capacity of SCAPs and down-regulated the expression of odontogenic-related markers. In conclusion, the results indicated that upregulation of NFIC activity in SCAPs may promote osteo/odontoblastic differentiation of SCAPs. (C) 2015 Elsevier Inc. All rights reserved.
引用
收藏
页码:259 / 266
页数:8
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