Long noncoding RNA MIR100HG regulates inflammatory response by interacting with RNA-binding protein Quaking in...

Area of Science:

• Molecular biology
• Immunology
• Periodontology

Background:

• Long noncoding RNAs (lncRNAs) are increasingly recognized as key regulators of periodontal inflammation.
• The specific role of lncRNA MIR100HG in periodontitis pathogenesis and its molecular interactions are not fully understood.

Purpose of the Study:

• To investigate the role of lncRNA MIR100HG in periodontitis.
• To elucidate the interaction between MIR100HG and the RNA-binding protein Quaking (QKI).

Main Methods:

• RNA sequencing and fluorescence in situ hybridization (FISH) were used to analyze MIR100HG expression and localization.
• In vitro studies involved stimulating human gingival fibroblasts (HGFs) with Porphyromonas gingivalis lipopolysaccharide (Pg.LPS).
• In vivo studies utilized a ligature-induced periodontitis mouse model, alongside RNA immunoprecipitation (RIP) and Western blotting to explore molecular mechanisms.

Main Results:

• MIR100HG was found to be downregulated in inflamed gingival tissues and localized in the nucleus of HGFs.
• MIR100HG knockdown attenuated inflammation in HGFs and mitigated alveolar bone loss in mice, while overexpression exacerbated inflammatory responses.
• MIR100HG interacts with QKI, forming a negative feedback loop that regulates nuclear factor kappa B (NF-κB) activation, thereby modulating periodontal inflammation.

Conclusions:

• MIR100HG is a crucial lncRNA in periodontitis, downregulated in both human and animal models.
• MIR100HG knockdown alleviates periodontal inflammation and bone loss through a QKI-mediated mechanism.
• MIR100HG represents a potential therapeutic target for managing periodontitis.