Key laboratory of Shaanxi Province for Craniofacial Precision Medicine Research & Department of Prosthodontics, College of Stomatology, Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Department of Prosthodontics, Digital Stomatological Engineering Center, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, China.
Mediators Inflamm. 2019 Sep 8;2019:1625381. doi: 10.1155/2019/1625381. eCollection 2019.
circRNA CDR1as (CDR1as) has been demonstrated to play important roles in a variety of inflammation-related diseases by acting as miRNA sponges. The present study is aimed at investigating the potential roles of CDR1as in the proliferation of human periodontal ligament stem cells (PDLSCs) under an inflammatory condition induced by -derived lipopolysaccharide (LPS). Human periodontal ligament cells (PDLCs) were isolated from periodontal ligament tissue, and PDLSCs were sorted from PDLCs based on the STRO-1 expression through fluorescence-activated cell sorting. We further found that CDR1as was significantly downregulated in LPS-treated PDLSCs compared to untreated cells, as well as in normal periodontal ligament tissues compared to periodontitis tissues. Knockdown of CDR1as promoted LPS-induced proliferative inhibition of PDLSCs, whereas overexpression of CDR1as alleviated the LPS-induced proliferative ability of PDLSCs. Mechanistically, CDR1as functioned as an miR-7 sponge to activate the ERK signal pathway to mediate the inhibition effect of LPS on cell proliferation. Taken together, our findings revealed the effects of the interacting pair of CDR1as/miR-7 on the proliferation ability of PDLSCs within their surrounding inflammatory microenvironment of periodontitis.
环状 RNA CDR1as（CDR1as）已被证明通过作为 miRNA 海绵在多种与炎症相关的疾病中发挥重要作用。本研究旨在探讨 CDR1as 在由脂多糖（LPS）诱导的炎症条件下对人牙周膜干细胞（PDLSCs）增殖的潜在作用。从牙周膜组织中分离出人牙周膜细胞（PDLCs），并通过荧光激活细胞分选基于 STRO-1 表达从 PDLCs 中分选 PDLSCs。我们进一步发现，与未处理的细胞相比，LPS 处理的 PDLSCs 中 CDR1as 显著下调，与正常牙周组织相比，牙周炎组织中 CDR1as 下调更为明显。CDR1as 的敲低促进了 LPS 诱导的 PDLSCs 增殖抑制，而过表达 CDR1as 则减轻了 LPS 诱导的 PDLSCs 增殖能力。机制上，CDR1as 作为 miR-7 的海绵体激活 ERK 信号通路，介导 LPS 对细胞增殖的抑制作用。综上所述，我们的研究结果揭示了 CDR1as/miR-7 相互作用对牙周炎周围炎症微环境中 PDLSCs 增殖能力的影响。
