LncRNA LBX2-AS1 exacerbates LPS-induced stress on periodontal ligament cells by activating the TLR2 signaling pathway through miR-654-3p

Periodontitis poses challenges in both early detection and late-stage treatment. The purpose of this study was to understand the role and mechanism of the lncRNA LBX2-AS1 in periodontitis. Baseline clinical data were collected from 107 patients in the periodontitis group and 107 participants in the periodontally healthy control group (HC). Expression of LBX2-AS1 in gingival crevicular fluid (GCF) was assessed using qRT-PCR. To verify the binding relationships between miR-654-3p, LBX2-AS1 and TLR2, dual luciferase reporter gene and pull-down assays were performed. Periodontal ligament cells (PDLCs) were stimulated with LPS to mimic periodontitis conditions. ELISA was used to measure TNF-α, IL-6, and IL-1β levels. ALP activity and RUNX2/OCN protein expression were detected to assess osteogenic differentiation. CCK-8 and flow cytometry were performed to analyze PDLCs proliferation and apoptosis. LBX2-AS1 and TLR2 were upregulated, while miR-654-3p was downregulated in periodontitis patients GCF. LBX2-AS1 could efficiently identify the onset of periodontitis. Downregulation of LBX2-AS1 inhibited inflammatory factor release, suppressed PDLCs proliferation, and differentiation, promoted apoptosis, and reversed LPS-induced damage to PDLCs. LBX2-AS1 negatively regulated miR-654-3p, and its downregulation counteracted the effects of LBX2-AS1 knockdown. As a target of miR-654-3p, TLR2 exacerbated LPS-induced inflammation and injury in PDLCs. miR-654-3p overexpression represses Myd88/NF-κB protein expression. Upregulation of LBX2-AS1 has the potential to be a marker for the development of periodontitis. miR-654-3p mediates the impact of LBX2-AS1 on LPS-stimulated inflammatory responses and cellular damage in PDLCs via the TLR2/Myd88/NF-κB signaling pathway.