Int J Stomatol

Int J Stomatol ›› 2020, Vol. 47 ›› Issue (2): 138-145.doi: 10.7518/gjkq.2020018

• Periodontitis • Previous Articles     Next Articles

Progress in research of non-coding RNAs in osteogenic differentiation of human periodontal ligament stem cells

Wang Runting1,2,Fang Fuchun1,2()   

  1. 1. Dept. of Stomatology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China
    2. School of Stomatology, Southern Medical University, Guangzhou 510515, China
  • Received:2019-06-14 Revised:2019-10-23 Online:2020-03-01 Published:2020-03-12
  • Contact: Fuchun Fang E-mail:fangfuchun520@163.com
  • Supported by:
    This study was supported by National Natural Science Foundation of China(81600882)

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Abstract:

Periodontitis is a common inflammatory disease that is characterised by progressive damage to dental supporting structure. Periodontitis is the main cause of tooth loss in adults in China. The aim of periodontal treatment is not only to control inflammation and prevent disease development but also to obtain periodontal regeneration. Human periodontal ligament stem cells (PDLSCs), which are capable of osteogenic differentiation, are expected to play important roles in clinical application of periodontal tissue repair and regeneration. Non-coding RNAs (ncRNAs) generally refer to RNAs that do not encode proteins. The continuous development of high-throughput detection techniques has allowed the identification of a large number of ncRNAs and their biological functions. Increasing numbers of ncRNAs have been reported to function in the pathogenesis of diseases at molecular and cellular levels. Therefore, research on ncRNAs can provide new insights into periodontal regeneration. This review focuses on the regulatory mechanism of several ncRNAs in the osteogenic differentiation of human PDLSCs.

Key words: non-coding RNA, periodontal regeneration, periodontal ligament stem cell, osteogenic differentiation

CLC Number: 

  • Q756

TrendMD: 

Tab 1

Regulation of ncRNAs on osteogenic differentiation of periodontal ligament stem cells"

名称 类型 诱导方式 调控水平 调控作用 可能的靶基因或作用通路 文献
miR-24-3p miRNA 矿化 转录后水平 抑制 靶向作用Smad5 [15]
miR-21 miRNA 矿化 转录后水平 抑制 靶向作用Smad5 [16]
矿化 转录后水平 抑制 miR-21/Spry1调控轴介导TNF-α对牙周膜干细胞的抑制成骨 [17]
作用
剪切力 转录后水平 抑制 靶向作用ACVR2B [29]
miR-203 miRNA 矿化 转录后水平 抑制 靶向作用RUNX2 [18]
miR-1305 miRNA 矿化 转录后水平 抑制 靶向作用RUNX2 [19]
miR-218 miRNA 矿化 转录后水平 抑制 靶向作用RUNX2 [20]
miR-214 miRNA 矿化 转录后水平 抑制 靶向作用ATF4 [21]
矿化 转录后水平 抑制 通过靶向作用β-连环蛋白1调节Wnt/β-连环蛋白信号通路 [22]
miR-17 miRNA 矿化 转录后水平 抑制 通过靶向作用TCF3调节经典Wnt信号通路 [23-24]
miR-31 miRNA 矿化 转录后水平 抑制 靶向作用Satb2 [25]
miR-200c miRNA 矿化 转录后水平 促进 抑制IL-6、IL-8和CCL-5 [26]
miR-543 miRNA 矿化 转录后水平 促进 靶向作用TOB2 [27]
miR-22 miRNA 矿化 转录后水平 促进 抑制HDAC6 [28]
名称 类型 诱导方式 调控水平 调控作用 可能的靶基因或作用通路 文献
MEG3 lncRNA 矿化 转录水平 抑制 与hnRNPK结合,影响BMP2转录 [37]
ANCR lncRNA 矿化 转录水平 抑制 通过调控GSK3β的表达抑制Wnt/β-连环蛋白信号通路,下调 [38]
RUNX2
矿化 转录后水平 抑制 ANCR/miR-758/Notch2 [40]
TUG1 lncRNA 矿化 转录水平 促进 Lin28A蛋白作为TUG1的RBP形成正性调控网络 [36]
PCAT1 lncRNA 矿化 转录后水平 促进 PCAT1/miR-106a-5p/BMP2 PCAT1/miR-106a-5p/E2F5前馈调 [41]
节网络
HIF1A-AS2 lncRNA 缺氧 转录后水平 促进 通过碱基配对与HIF-1α形成双链RNA,提高蛋白质翻译水平 [42]
CDR1 circRNA 矿化 转录后水平 促进 竞争性结合miR-7,使GDF5上调、Smad1/5/8及p38MAPK [46]
磷酸化
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