Impacts of long noncoding RNA MALAT1 on LPS-induced periodontitis via modulating miR-155/SIRT1 axis

Objectives: Periodontitis, a dental disease that causes inflammation of gums is triggered by a bacterial infection. Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (lncRNA MALAT1) has been reported to participate in inflammatory diseases. In the present study, we investigated the effects of lncRNA MALAT1 on periodontal ligament cells (PDLCs) with lipopolysaccharide (LPS) induction. Methods: MALAT1, microRNA-155 (miR-155), Sirtuin 1 (SIRT1), Bax, and Bcl-2 RNA expressions were detected by using real-time quantitative polymerase chain reaction (RT-qPCR). PDLC viability and apoptosis were assessed by using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide tetrazolium salt (MTT) assay and flow cytometry. Enzyme-linked immunosorbent assay (ELISA) assessed secretions of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Luciferase reporter test was applied for confirming the binding of miR-155 with MALAT1 and SIRT1, respectively. Results: Overexpression of MALAT1 facilitated the LPS-induced periodontitis while MALAT1 suppression restrained LPS-induced injury. Also, miR-155 was expressed in LPS-induced PDLCs. Moreover, MALAT1 negatively regulated miR-155 followed by the up-regulation of SIRT1 which in turn reduced the inflammation in LPS-induced PDLCs. Conclusions: We concluded that upregulated lncRNA MALAT1 could accelerate periodontitis through the regulation of miR-155/SIRT1. Our findings suggested a novel MALAT1/miR-155/SIRT1 pathway for the treatment of periodontitis.