Role of Long Non-Coding RNA GUSBP11 in Chronic Periodontitis Through Regulation of miR-185-5p: A Retrospective Cohort Study.

PURPOSE: Previous studies have shown that long non-coding RNA GUSBP11 is abnormally expressed in patients with periodontitis, but the specific mechanism remains to be investigated. The purpose of this study was to explore the role of GUSBP11/miR-185-5p in chronic periodontitis (CP) and its potential mechanism, so as to provide a basis for elucidating the pathogenesis of CP.

PATIENTS AND

METHODS

The expression trends of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients and control group were analyzed by RT-qPCR. Human gingival fibroblasts (HGF) induced by 10μg/mL LPS were used to construct CP cell models in vitro. The level of intracellular gene expression is regulated by cell transfection. The cell viability of HGF was evaluated by CCK-8 method, and the expression of HGF inflammatory factors was evaluated by ELISA. The targeting relationship between GUSBP11 and miR-185-5p was confirmed by luciferase reporter gene. The target genes of miR-185-5p were predicted using an online database, and the intersection target genes were obtained by constructing Venn diagram. Then GO analysis and KEGG pathway enrichment analysis were performed.

RESULTS

Compared with the control group, the expression levels of GUSBP11 and miR-185-5p in gingival crevicular fluid of CP patients were up-regulated and down-regulated, respectively (P < 0.001). The levels of GUSBP11 and miR-185-5p increased and decreased with the severity of CP, respectively (P < 0.01). LPS induces the decrease of HGF activity and the activation of inflammatory response, and the decrease of GUSBP11 may prevent the adverse effect of LPS on HGF (P < 0.001). Dual luciferase reporter genes showed that miR-185-5p interacts with GUSBP11. The increase of miR-185-5p also significantly improved the negative effect of LPS induction on HGF (P < 0.001).

CONCLUSION

GUSBP11 promotes the inflammatory response and proliferation inhibition of human gingival fibroblasts induced by LPS by down-regulating miR-185-5p, thus promoting the development of CP.