Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction

Abstract

Abstract Background Periodontitis is a common oral inflammatory disease, and lipopolysaccharide (LPS) is a key risk factor in periodontitis pathology. Here, we used LPS‐induced periodontal ligament cells (PDLCs) to explore the molecular mechanism of periodontitis. Methods Cell viability, proliferation, and apoptosis were analyzed by Cell Counting Kit‐8, 5‐ethynyl‐20‐deoxyuridine (EDU), and flow cytometry assays, respectively. Apart from that, their targeting relationship was validated using dual‐luciferase reporter and RNA‐pull down. Results Circular RNA_0138960 (circ_0138960) was notably upregulated in periodontitis sufferers (p < .001) and LPS‐disposed PDLCs (p < .05). LPS exposure dampened PDLC proliferation, and promoted apoptosis and inflammation (p < .05). Circ_0138960 acted as a microRNA sponge for miR‐518a‐5p to affect histone deacetylase 6 (HDAC6) expression. Circ_0138960 absence‐mediated protective effects in LPS‐induced PDLCs were largely abrogated via silencing miR‐518a‐5p or HDAC6 overexpression (p < .05). Conclusion Circ_0138960 promoted LPS‐induced dysfunction in PDLCs by targeting miR‐518a‐5p/HDAC6 axis, which provided novel potential therapeutic targets for periodontitis.

Keywords

• circ_0138960
• HDAC6
• lipopolysaccharide
• miR‐518a‐5p
• periodontal ligament cells
• periodontitis