Circ_0087199 depletion attenuates lipopolysaccharides‐induced human periodontal ligament cell injury through the miR‐527/TLR4 axis

Abstract

AbstractBackgroundCircular RNAs participate in the development of periodontitis. The present work aims to reveal the role and mechanism of circ_0087199 in human periodontal ligament cell (PDLC) injury during periodontitis.MethodsPDLCs were treated with lipopolysaccharides (LPS) to establish a periodontitis cell model. Quantitative real‐time polymerase chain reaction was used to detect the expression of circ_0087199, miR‐527, toll‐like receptor 4 (TLR4). Western blot analysis assay was performed to assess protein expression. Cell viability, proliferation, apoptosis and inflammation were investigated by cell counting kit‐8, EdU assay, flow cytometry and enzyme‐linked immunosorbent assay, respectively. Oxidative stress was evaluated by malondialdehyde assay kit and superoxide dismutase activity assay kit. The interaction between miR‐527 and circ_0087199 or TLR4 was confirmed by a dual‐luciferase reporter assay.ResultsCirc_0087199 and TLR4 expression levels were significantly increased, while miR‐527 was decreased in the periodontal ligament tissues of periodontitis patients and LPS‐stimulated PDLCs when compared with controls. LPS treatment inhibited cell viability and proliferation but induced cell apoptosis, inflammation and oxidative stress, whereas these effects were attenuated after circ_0087199 knockdown. Circ_0087199 bound to miR‐527 and regulated LPS‐caused PDLC damage by targeting miR‐527. Additionally, the overexpression of TLR4, a target gene of miR‐527, rescued miR‐527 mimic‐mediated effects on LPS‐treated PDLCs. Further, the regulation of circ_0087199 toward TLR4 involved miR‐527.ConclusionCirc_0087199 knockdown attenuated LPS‐induced apoptosis, inflammation and oxidative stress of PDLCs by regulating the miR‐527/TLR4 pathway.