LncRNA TUG1 mediates lipopolysaccharide-induced proliferative inhibition and apoptosis of human periodontal ligament cells by sponging miR-132.

Abstract

Emerging evidence shows that the long noncoding RNA taurine-upregulated gene 1 (TUG1) plays pivotal roles in regulating biological properties and functions of parenchyma cells in various types of disease processes. However, the mechanism underlying the effects of TUG1 on cell proliferation and apoptosis of human periodontal ligament cells (PDLCs) in periodontitis is undefined. In this study, we explored the functions of TUG1 and its underlying mechanisms in the inflammatory process induced by Porphyromonas gingivalis-derived lipopolysaccharide (LPS) in PDLCs. Our results showed that TUG1 had a decreased expression in both periodontal ligament (PDL) tissues with periodontitis and PDLCs under a LPS-induced inflammatory condition, and TUG1 expression was negatively correlated with miR-132 expression in periodontitis-affected PDL tissues. Furthermore, we found that TUG1 overexpression in PDLCs alleviated LPS-induced proliferative inhibition and apoptosis promotion, while TUG1 knockdown had the opposite effect. In addition, miR-132 inhibitor alleviated TUG1 knockdown-induced inhibition of proliferation and increase of apoptosis in PDLCs under inflammatory conditions induced by LPS. These findings indicated that TUG1 has an enormous potential in regulating cell proliferation and apoptosis of PDLCs during periodontitis and may provide an effective therapeutic target for periodontitis to reduce the damage caused by inflammatory reactions.