TET1 knockdown inhibits the odontogenic differentiation potential of human dental pulp cells

被引:26
作者
Rao, Li-Jia [1 ,2 ]
Yi, Bai-Cheng [1 ]
Li, Qi-Meng [1 ]
Xu, Qiong [1 ]
机构
[1] Sun Yat Sen Univ, Guangdong Prov Key Lab Stomatol, Guanghua Sch Stomatol, 56 Ling Yuan Xi Rd, Guangzhou 510055, Guangdong, Peoples R China
[2] Guangdong Med Coll, Nanshan Affiliated Hosp, Dept Stomatol, Shenzhen, Peoples R China
关键词
DNA demethylation; human dental pulp cell; knockdown; odontogenic differentiation; ten-eleven translocation 1; EMBRYONIC STEM-CELLS; DNA DEMETHYLATION DYNAMICS; MAMMALIAN DNA; 5-HYDROXYMETHYLCYTOSINE; METHYLATION; PROTEINS; 5-CARBOXYLCYTOSINE; 5-FORMYLCYTOSINE; 5-METHYLCYTOSINE; PROLIFERATION;
D O I
10.1038/ijos.2016.4
中图分类号
R78 [口腔科学];
学科分类号
1003 ;
摘要
Human dental pulp cells (hDPCs) possess the capacity to differentiate into odontoblast-like cells and generate reparative dentin in response to exogenous stimuli or injury. Ten-eleven translocation 1 (TET1) is a novel DNA methyldioxygenase that plays an important role in the promotion of DNA demethylation and transcriptional regulation in several cell lines. However, the role of TET1 in the biological functions of hDPCs is unknown. To investigate the effect of TET1 on the proliferation and odontogenic differentiation potential of hDPCs, a recombinant shRNA lentiviral vector was used to knock down TET1 expression in hDPCs. Following TET1 knockdown, TET1 was significantly downregulated at both the mRNA and protein levels. Proliferation of the hDPCs was suppressed in the TET1 knockdown groups. Alkaline phosphatase activity, the formation of mineralized nodules, and the expression levels of DSPP and DMP1 were all reduced in the TET1-knockdown hDPCs undergoing odontogenic differentiation. Based on these results, we concluded that TET1 knockdown can prevent the proliferation and odontogenic differentiation of hDPCs, which suggests that TET1 may play an important role in dental pulp repair and regeneration.
引用
收藏
页码:110 / 116
页数:7
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