Mechanism of the lncRNA-FGD5-AS1/miR-383-5p/SOCS3 signaling axis in periodontitis

Background lncRNAs served as crucial regulators in the pathogenesis and advancement of periodontitis. This study aimed to investigate whether lncRNA-FGD5-AS1 affects the proliferation and inflammatory response of LPS-induced HPDLSCs in vitro by regulating the miR-383-5p/SOCS3 axis. Method To set up an in vitro model of inflammation, HPDLSCs were treated with LPS. Cell proliferation, viability, gene expression (FGD5-AS1, miR-383-5p, and SOCS3), SOCS3 protein expression, and inflammatory cytokine levels were assessed by EdU staining, CCK-8, RT-qPCR, Western blot, and ELISA, respectively. Bioinformatics analysis, dual-luciferase reporter assays, RIP-qPCR, and RNA pull-down assays were further combined to verify the targeting relationships between miR-383-5p and SOCS3, and between FGD5-AS1 and miR-383-5p. Finally, oe-FGD5-AS1 and miR-383-5p mimic cell models were constructed to confirm that FGD5-AS1 regulated LPS-induced inflammatory injury via the miR-383-5p/SOCS3 axis. Results LPS exhibited a dose-dependent inhibitory effect on both the mRNA and protein levels of SOCS3 in HPDLSCs, and also inhibited cell proliferation. SOCS3 overexpression, in functional rescue experiments, was shown to lower the production of TNF-α, IL-1β, and IL-6 and rescue cell proliferation. At the mechanistic level, miR-383-5p directly targeted and downregulated SOCS3. Conversely, FGD5-AS1 served as a ceRNA that upregulated SOCS3 by sponging miR-383-5p. Functional experiments verified that FGD5-AS1 adsorbed miR-383-5p to relieve its inhibitory effect on SOCS3, thereby alleviating the inflammatory response induced by LPS, and exogenous addition of miR-383-5p could reverse this protective effect. Conclusion By acting as a molecular sponge for miR-383-5p, FGD5-AS1 upregulates SOCS3 expression, thereby suppressing inflammation and enhancing the proliferative capacity of HPDLSCs in an in vitro model of LPS-induced periodontitis. These findings provide a novel theoretical framework for the epigenetic regulation of periodontitis and suggest that this axis may serve as a potential therapeutic target, which warrants further validation in appropriate in vivo models and clinical studies.