Related Experiment Videos
circMYO9B affects the progression of periodontitis by targeting the miR-4731-5p/USP15 axis
Huimin Xie1, Huiling Qin2,3, Zhengyi Chu4
1Department of Orthodontics, Affiliated Nantong Stomatological Hospital of Nantong University, Nantong, China.
Purpose:
Periodontitis is a common oral disease characterized by inflammation and destruction of periodontal tissues. Competitive endogenous RNAs (ceRNAs) are known to regulate inflammatory responses. This study aimed to investigate the role of circular RNA MYO9B (circMYO9B), as a potential ceRNA, in the progression of periodontitis and to elucidate its underlying regulatory mechanism.
Methods:
This study included 69 healthy controls and 71 patients with periodontitis. Lipopolysaccharide (LPS)-treated periodontal ligament cells (PDLCs) were used as an in vitro model of periodontitis. Reverse transcription-quantitative polymerase chain reaction was performed to quantify circMYO9B, miR-4731-5p, and ubiquitin-specific peptidase 15 (USP15) expression, while enzyme-linked immunosorbent assays were used to measure inflammatory cytokine levels. Cell proliferation, migration, and apoptosis were assessed using the Cell Counting Kit-8 assay, Transwell migration assay, and flow cytometry, respectively. Dual-luciferase reporter assays were conducted to validate the interactions among circMYO9B, miR-4731-5p, and USP15.
Results:
circMYO9B expression was significantly elevated in the gingival crevicular fluid of patients with periodontitis and in LPS-treated PDLCs. Receiver operating characteristic curve analysis demonstrated that circMYO9B had diagnostic potential for periodontitis (area under the curve: 0.919). LPS stimulation reduced PDLC viability and migratory capacity while increasing inflammatory cytokine production and apoptosis. circMYO9B directly targeted and negatively regulated miR-4731-5p. Silencing circMYO9B significantly attenuated LPS-induced PDLC dysfunction, whereas inhibition of miR-4731-5p abolished the protective effects of circMYO9B knockdown. USP15 was identified as a direct downstream target of miR-4731-5p: overexpression of miR-4731-5p alleviated LPS-induced cellular injury in PDLCs, but this protective effect was markedly reversed by concomitant USP15 overexpression.
Conclusions:
circMYO9B is associated with periodontitis progression through the miR-4731-5p/USP15 regulatory axis, suggesting its potential utility as a therapeutic target in periodontitis.
