FAM30A Induces Inflammation and Oxidative Damage in PDLSCs by Targeting miR-424-5p

To investigate the diagnostic value and regulatory role of FAM30A in patients with chronic periodontitis (CP).

The study included 104 CP patients. Saliva and periodontal ligament tissue samples were stored at -80°C. Logistic regression predicted risk factors for CP. Periodontal ligament stem cells (PDLSCs) were stimulated with 100 ng/mL LPS to establish an in vitro model. RT-qPCR assessed gene expression. CCK-8 and flow cytometry evaluated cell proliferation and apoptosis. ELISA measured inflammatory cytokine expression, while kits quantified oxidative stress products. Dual luciferase reporter assays and RNA immunoprecipitation examined gene-target relationships.

FAM30A was upregulated in saliva and periodontal ligament tissue from CP patients. FAM30A demonstrated diagnostic value in both sample types and was identified as a risk factor for CP. LPS stimulation increased FAM30A expression in cells. si-FAM30A promoted cell proliferation, reduced apoptosis, and suppressed inflammatory and oxidative stress levels. miR-424-5p was downregulated in CP patients. Furthermore, FAM30A competitively binds miR-424-5p to modulate PDLSCs' function. Transfection with miR inhibitor counteracts si- FAM30A-induced cellular dysfunction and inflammatory responses.

FAM30A induces CP by targeting miR-424-5p to inhibit PDLSCs proliferation, promote apoptosis, and increase inflammatory and oxidative stress levels.