Maternally-Expressed Gene 3 (MEG3)/miR-143-3p Regulates Injury to Periodontal Ligament Cells by Mediating the AKT/Inhibitory κB Kinase (IKK) Pathway

Abstract

Background

Dysregulated long noncoding RNAs (lncRNAs) are implicated in periodontitis development. Nevertheless, the role and mechanism of lncRNA maternally-expressed gene 3 (MEG3) in periodontitis progression remain unclear. This study aimed to explore how and whether MEG3 affect viability, apoptosis, and inflammatory response in lipopolysaccharide (LPS)-treated periodontal ligament cells (PDLCs).

Material/Methods

Periodontal ligament tissues were collected from periodontitis patients or normal individuals. PDLCs were obtained from normal periodontal ligament and treated with lipopolysaccharide (LPS). LPS-induced PDLCs injury was assessed via viability, apoptosis and inflammatory response using Cell Counting Kit-8, flow cytometry, quantitative reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay, and Western blot. The levels of MEG3 and microRNA (miR)-143-3p were examined via quantitative reverse transcription polymerase chain reaction. The protein kinase B(AKT)/inhibitory κB kinase (IKK) pathway was analyzed via Western blot. The target correlation of MEG3 and miR-143-3p was determined through dual-luciferase reporter analysis.

Results

MEG3 level was decreased and miR-143-3p level was upregulated in periodontitis and LPS-treated PDLCs. MEG3 overexpression or miR-143-3p knockdown alleviated LPS-induced viability inhibition, apoptosis promotion, and inflammatory response. MEG3 was a sponge for miR-143-3p. miR-143-3p overexpression weakened the effect of MEG3 on LPS-induced injury. MEG3 overexpression inhibited the activation of AKT/IKK pathway by sponging miR-143-3p in LPS-treated PDLCs.

Conclusions

MEG3 overexpression inhibited LPS-induced injury in PDLCs by inactivating the AKT/IKK pathway via sponging miR-143-3p, providing a potential target for treatment of periodontitis.