Circ_0138960 contributes to lipopolysaccharide‐induced periodontal ligament cell dysfunction. Issue 12 (7th November 2022)

• Record Type: Journal Article
• Authors: Li, Shuangshuang; Xu, Huilin; Li, Yuanyuan; Li, Ruijing
• Is Part Of: Immunity, inflammation and disease. Volume 10:Issue 12(2022)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2022-11-07
• Subjects: circ_0138960 -- HDAC6 -- lipopolysaccharide -- miR‐518a‐5p -- periodontal ligament cells -- periodontitis; Immunology -- Periodicals; Immunity -- Periodicals; Inflammation -- Periodicals; 616.079
• DOI: 10.1002/iid3.732
• Languages: English
• ISSNs: 2050-4527

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. Abstract : Please designate which figure should be used for the graphical table of contents and considered for the publication cover.