Abstract
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. 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. 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 microRNAsponge 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). Circ_0138960 promoted LPS-induced dysfunction in PDLCs by targeting miR-518a-5p/HDAC6 axis, which provided novel potential therapeutic targets for periodontitis.
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