Abstract
BACKGROUND: The aim of this study is to investigate whether LINC00673 and leptin are associated with osteogenesis of periodontal ligament stem cells in the microenvironment of advanced glycation end products. METHODS: LINC00673 expression was detected in PDLSCs by qRT-PCR performed during osteogenic differentiation. By using alkaline phosphatase and Alizarin red S staining, we were able to confirm the role of LINC00673 in regulating osteogenesis in PDLSCs. Assays were performed on nude mice to test bone regeneration in the dorsal region to investigate MiR-188-3p's binding to LINC00673 and leptin (LEP). Western blot was used to detect osteoblast markers (COL1, ALP and RUNX2). RESULTS: As predicted, miR-188-3p interacts with LINC00673 directly, and miR-188-3p overexpression increases osteogenic differentiation. However, overexpression of LINC00673 reversed this effect, suggesting that LINC00673 functions as a competing endogenous RNA for miR-188-3p. A regulatory network formed by LINC00673 and miR-188-3p regulates the expression of LEP, a gene that inhibits the canonical Wnt pathway, reducing bone formation in PDLSCs. CONCLUSIONS: PDLSCs differentiate osteogenically as a result of a regulatory network between lncRNA and miRNA (microRNA), which may serve as a therapeutic target for diabetes-related periodontitis.