Department of Laboratory Medicine, Key Laboratory of Diagnostic Medicine (Ministry of Education), Chongqing Medical University, Chongqing, China.
School of Computer Science, Chongqing Institute of Engineering, Chongqing, China.
J Periodontal Res. 2020 Oct;55(5):631-641. doi: 10.1111/jre.12749. Epub 2020 Apr 2.
Accumulating findings revealed that long noncoding RNAs (lncRNAs) are crucial regulator molecules in the progression of periodontitis. This study aimed to investigate the biological roles and mechanisms of lncRNA-01126 in the progression of periodontitis.
RT-qPCR was used to detect the levels of lncRNA-01126 in gingival tissues and human periodontal ligament cells (hPDLCs). Cell transfection experiments were performed to knock down or overexpress the level of lncRNA-01126 in hPDLCs. Cell Counting Kit-8, wound-healing assay, transwell assay, and flow cytometric analysis were used to evaluate the function of lncRNA-01126 in the progression of periodontitis. Finally, the signaling pathway was assessed by western blot.
LncRNA microarray discovered that lncRNA-01126 was the most significantly increased lncRNA in periodontitis patients. LncRNA-01126 markedly increased in the gingival tissues of periodontitis mice and in the hPDLCs treated with lipopolysaccharide of Porphyromonas Gingivalis (LPS-PG). Furthermore, in vitro experiments showed that lncRNA-01126 dramatically suppressed the migration of hPDLCs through MEK/ERK signaling pathway.
LncRNA-01126 plays a crucial role in inhibiting the migration of hPDLCs through MEK/ERK signaling pathway.
越来越多的研究结果表明,长链非编码 RNA(lncRNA)是牙周炎进展过程中的关键调节分子。本研究旨在探讨 lncRNA-01126 在牙周炎进展中的生物学作用和机制。
采用 RT-qPCR 检测龈组织和人牙周膜细胞(hPDLCs)中 lncRNA-01126 的水平。通过细胞转染实验下调或上调 hPDLCs 中 lncRNA-01126 的水平。采用细胞计数试剂盒-8、划痕愈合实验、Transwell 实验和流式细胞术分析评估 lncRNA-01126 在牙周炎进展中的功能。最后,通过 Western blot 评估信号通路。
lncRNA 芯片发现 lncRNA-01126 是牙周炎患者中表达增加最显著的 lncRNA。牙周炎小鼠的龈组织和经牙龈卟啉单胞菌脂多糖(LPS-PG)处理的 hPDLCs 中 lncRNA-01126 明显增加。此外,体外实验表明 lncRNA-01126 通过 MEK/ERK 信号通路显著抑制 hPDLCs 的迁移。
lncRNA-01126 通过 MEK/ERK 信号通路在抑制 hPDLCs 的迁移中发挥重要作用。