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

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