MicroRNA-212-5p regulates the inflammatory response of periodontal ligament cells by targeting myeloid differentiation factor 88

This study was aimed to investigate the effects of microRNA-212-5p (miR-212-5p) and myeloid differentiation factor 88 (Myd88) in Porphyromonas gingivalis lipopolysaccharide (P. gingivalis LPS)-challenged human periodontal ligament cells (PDLCs). The levels of miR-212-5p and Myd88 in PDLCs were determined via quantitative real-time Polymerase Chain Reaction. Cell viability and pro-inflammatory cytokines were assessed using MTT assay and enzyme-linked immunosorbent assay. Bioinformatics and luciferase reporter gene assay were employed to explore the interaction between miR-212-5p and Myd88. Moreover, the activation of p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-B signal pathways were testified via western blot analysis. MiR-212-5p was downregulated following stimulation of P. gingivalis LPS. Overexpression of miR-212-5p elevated the cell viability and reduced the secretion of pro-inflammatory cytokines. Myd88 is a target of miR-212-5p. Notably, pcDNA3.1-Myd88 reversed the anti-inflammatory effect of miR-212-5p overexpression. Likewise, miR-212-5p mimic inhibited the activation of p38 MAPK and nuclear factor kappa-B, whereas pcDNA3.1-Myd88 abrogated the effect of miR-212-5p mimic. MiR-212-5p inhibited the inflammatory response in PDLCs by targeting Myd88, which may involve the inactivation of p38 MAPK and nuclear factor kappa-B.