| Popis: |
Periodontitis and diabetes are both chronic diseases with a complex bidi- rectional relationship. Diabetes increases the risk of periodontitis by two to three times when compared to people who do not have diabetes. In this study, we used microarray analysis to identify differentially expressed lncRNAs and mRNAs in response to advanced glycosylation end prod- ucts (AGEs) and conventional osteogenic induction, and we identified LINC00673 as the target. LINC00673, a recently discovered lncRNA, has been studied in various cancers. However, the function and regulatory mechanism of LINC00673 in PDLSCs exposed to the AGEs microenvi- ronment have never been fully explored. Following that, we predicted an interaction between LINC00673 and miR188-3p and confirmed the direct binding sites of miR-188-3p on LINC00673. MiR-188-3p overexpres- sion resulted in increased osteogenic differentiation, whereas LINC00673 overexpression reversed its suppression, indicating that LINC00673 acts as a competing endogenous RNA for miR-188-3p. By suppressing one another, LINC00673 and miR-188-3p form a network that controls LEP, its target gene. By inhibiting the canonical Wnt pathway, LEP decreased bone formation in PDLSCs. In conclusion, our findings provide new evi- dence that this lncRNA-miRNA (microRNA) regulatory network plays an important role in the osteogenic differentiation of PDLSCs and has the potential to be a therapeutic target for diabetes-related periodontitis. |
