a Department of Endodontics, Shenzhen Stomatological Hospital, Southern Medical University , Shenzhen , China.
b Shenzhen Stomatological Hospital, Southern Medical University , Shenzhen , China.
Artif Cells Nanomed Biotechnol. 2019 Dec;47(1):2098-2106. doi: 10.1080/21691401.2019.1620256.
Periodontitis refers to the inflammation of gums and the surrounding structures and caused by a bacterial infection. The infection occurs owing to poor oral hygiene and could destroy the bone and the gum over time if left untreated. The present study identified the involvement of a key long noncoding RNA (lncRNA), i.e. FGD5-AS1, in the pathogenesis of periodontitis by assessing its expression in the gingival tissues of patients diagnosed with chronic periodontitis (CP). Overexpression of FGD5-AS1 in primary human periodontal ligament cells (PDLCs) significantly reduced the lipopolysaccharide (LPS)-induced periodontitis, whereas its suppression aggravated this injury. Moreover, the miR-142-3p was markedly expressed in the gingival samples of patients diagnosed with CP and LPS-induced PDLCs. We found that the FGD5-AS1-mediated reduction in the inflammation was mediated through downside regulation of miR-142-3p, as evident from the upregulation of SOCS6, a target gene of miR-142-3p. Furthermore, the association between FGD5-AS1 and NF-κB pathway was detected. FGD5-AS1 was found to protect against LPS-stimulated PDLC injury through restraining the NF-κB signals. Based on these findings, we conclude that up-regulation of lncRNA FGD5-AS1 could protect against periodontitis via regulating the miR-142-3p/SOCS6/NF-κB signals. Therefore, the FGD5-AS1/miR-142-3p/SOCS6 axis may act as an important indicator in explaining the pathogenesis of periodontitis.
牙周炎是指牙龈和周围结构的炎症，由细菌感染引起。这种感染是由于口腔卫生不良引起的，如果不治疗，随着时间的推移，它会破坏骨骼和牙龈。本研究通过评估慢性牙周炎（CP）患者牙龈组织中关键长链非编码 RNA（lncRNA），即 FGD5-AS1 的表达，来确定其在牙周炎发病机制中的作用。在原代人牙周韧带细胞（PDLCs）中过表达 FGD5-AS1 显著减轻了脂多糖（LPS）诱导的牙周炎，而其抑制作用则加重了这种损伤。此外，miR-142-3p 在 CP 患者和 LPS 诱导的 PDLCs 的牙龈样本中明显表达。我们发现，FGD5-AS1 介导的炎症减少是通过下调 miR-142-3p 介导的，因为 miR-142-3p 的靶基因 SOCS6 上调。此外，还检测到 FGD5-AS1 与 NF-κB 通路之间的关联。FGD5-AS1 被发现通过抑制 NF-κB 信号来保护 LPS 刺激的 PDLC 损伤。基于这些发现，我们得出结论，上调 lncRNA FGD5-AS1 可以通过调节 miR-142-3p/SOCS6/NF-κB 信号来预防牙周炎。因此，FGD5-AS1/miR-142-3p/SOCS6 轴可能作为解释牙周炎发病机制的重要指标。
