Odontoblast-like MDPC-23 cells function as odontoclasts with RANKL/M-CSF induction

被引:12
|
作者
Duan, Xiaohong [1 ]
Yang, Ting [1 ]
Zhang, Yanli [1 ]
Wen, Xuan [1 ]
Xue, Yang [1 ]
Zhou, Mi [1 ]
机构
[1] Fourth Mil Med Univ, Sch Stomatol, Dept Oral Biol, Xian 710032, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
RANKL; M-CSF; Odontoclast; Odontoblast; Chloride channel; HUMAN DECIDUOUS TEETH; OSTEOCLAST DIFFERENTIATION; DENTAL-PULP; STEM-CELLS; IPS CELLS; PRECURSORS; EXPRESSION; RESORPTION; CYTOKINE; LIGAND;
D O I
10.1016/j.archoralbio.2012.05.014
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
The identity of odontoclast precursors and the molecular mechanism by which odontoclasts resorb dentine remain unclear. MDPC-23 cells were derived from dental papilla cells and possessed odontoblast characteristics such as expressing dentine sialophosphoprotein (Dspp) and dentine matrix acidic phosphoprotein 1 (Dmp1). Here we induced MDPC-23 cells to have an odontoclast-like function with receptor activator of nuclear factor-kappa B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). We found that tartrate-resistant acid phosphatase (TRAP)-positive cells, TRAP-positive multinucleated cells on the dentine slice were significantly increased in RANKL/M-CSF-induced cells. Osteoclast-specific genes such as Trap, osteopetrosis-associated transmembrane protein 1 (Ostm1), chloride channel 7 (Clcn7), cathepsin K (Ctsk) as well as osteoclast-specific transcription factor and microphthalmia transcription factor (MITF) were up-regulated in the treated cells, whilst the messenger RNA (mRNA) levels of Dspp, Dmp1 and Opg were reduced in the induced cells. The intracellular environment became more acidic in the RANKL/M-CSF treatment group, which resulted in more absorptive pits in dentine slices. We suggested that RANKL/ M-CSF might induce odontoblast-like MDPC-23 cells to differentiate into odontoclast-like cells or function as odontoclasts. Our data might provide a new explanation for the precursors of odontoclast and root resorption. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:272 / 278
页数:7
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