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Updated: May 14, 2025
Robust Ligature-Induced Model of Murine Periodontitis for the Evaluation of Oral Neutrophils
Published on: January 21, 2020
hsa_circ_0095812 accelerates periodontitis progression by adsorbing miR-485-3p-mediated THBS1 expression
XiaoTing Xie1, RuiTing Li1, FangLin Mi1
1North Sichuan Medical College, Nanchong City, Sichuan Province, PR China.
Insights
Circular RNA circLRRC4C promotes periodontitis by sponging miR-485-3p, leading to increased Thrombospondin-1 (THBS1) expression and inflammation. Suppressing circLRRC4C alleviates periodontitis in mice.
Area of Science:
- Oral Biology
- Molecular Biology
- Immunology
Background:
- Periodontitis is a prevalent inflammatory disease affecting tooth-supporting structures.
- Circular RNAs (circRNAs) are emerging as key regulators in various diseases, including inflammatory conditions.
- The specific role of circLRRC4C in periodontitis pathogenesis remains largely unexplored.
Purpose of the Study:
- To investigate the role of hsa_circ_0095812 (circLRRC4C) in periodontitis.
- To elucidate the underlying molecular mechanism involving miR-485-3p and Thrombospondin-1 (THBS1).
Main Methods:
- Analysis of circLRRC4C expression in human periodontitis tissues and lipopolysaccharide (LPS)-stimulated Periodontal Ligament Cells (PDLCs).
- In vitro studies assessing cell viability, inflammation, apoptosis, and pyroptosis following circLRRC4C manipulation.
- In vivo studies using a mouse model of periodontitis with targeted circLRRC4C intervention.
- Molecular analyses including qRT-PCR, Western blot, and miRNA-sponge assays to determine regulatory relationships.
Main Results:
- CircLRRC4C was significantly upregulated in periodontitis tissues and LPS-treated PDLCs.
- Downregulation of circLRRC4C reduced LPS-induced inflammation, apoptosis, and pyroptosis while improving cell viability.
- CircLRRC4C functions as a molecular sponge for miR-485-3p, and THBS1 was identified as a target gene of miR-485-3p.
- The circLRRC4C/miR-485-3p/THBS1 axis was found to exacerbate periodontitis, and its suppression ameliorated the condition in a mouse model.
Conclusions:
- CircLRRC4C promotes periodontitis progression by sponging miR-485-3p, thereby upregulating Thrombospondin-1 (THBS1) expression.
- Targeting circLRRC4C offers a potential therapeutic strategy for periodontitis.
Objective:
To explore the role of hsa_circ_0095812 (circLRRC4C) in periodontitis and its mechanism with miR-485-3p and Thrombospondin-1 (THBS1).
Methods:
Periodontal tissues were collected from periodontitis patients. Periodontal Ligament Cells (PDLCs) were stimulated with Lipopolysaccharide (LPS) and transfected. Cell viability, inflammation, apoptosis, and pyroptosis were analyzed. A mouse model of periodontitis was constructed and injected with a lentiviral plasmid vector targeting circLRRC4C. Immunohistochemistry was performed on the periodontal tissue of model mice. The relevant expression level of genes was measured via real-time reverse transcriptase-polymerase chain reaction or Western blot. The relationship between circLRRC4C and THBS1 with miR-485-3p was analyzed.
Results:
CircLRRC4C was highly expressed in periodontitis tissues of patients and LPS-treated PDLCs. Downregulating circLRRC4C attenuated LPS-induced PDLC inflammation, apoptosis and pyroptosis and recovered cellular viability. CircLRRC4C acted as a sponge for miR-485-3p. CircLRRC4C affected LPS-induced PDLC apoptosis, pyroptosis and inflammation by regulating miR-485-3p. THBS1 was the target gene of miR-485-3p. Inhibition of THBS1 effectively improved LPS-induced periodontitis. CircLRRC4C aggravated LPS-induced PDLC apoptosis, pyroptosis and inflammation by regulating the miR-485-3p/THBS1 axis. Suppressing circLRRC4C effectively improved periodontitis in mice.
Conclusion:
CircLRRC4C induces periodontitis progression by adsorbing miR-485-3p-mediated THBS1 expression.
