Long non-coding RNA TMPO-AS1 promotes chronic periodontitis progression by negatively regulating miR-383-5p expression in human periodontal stromal cells.

OBJECTIVES

This study aimed to investigate the molecular mechanisms by which TMPO-AS1 regulates inflammation and osteogenic differentiation in chronic periodontitis (CP).

DESIGN

125 CP patients and 125 healthy controls were enrolled. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect serum levels of TMPO-AS1 and microRNA-383-5p (miR-383-5p). Human periodontal ligament stromal cells (hPDLSCs) were induced to undergo in vitro osteogenic differentiation. An inflammatory model was established using lipopolysaccharide (LPS). Using cell counting kit-8 (CCK-8) assays, alkaline phosphatase (ALP) activity assays, enzyme-linked immunosorbent assay (ELISA), RNA immunoprecipitation (RIP), and dual luciferase reporter assays to investigate the targeted regulatory relationship and biological functions of TMPO-AS1 and miR-383-5p.

RESULTS

Serum TMPO-AS1 expression was significantly elevated in CP patients and positively correlated with inflammatory cytokines and periodontal clinical indicators, demonstrating potential as a candidate auxiliary diagnostic indicator for CP. LPS exerted a concentration-dependent upregulation of TMPO-AS1 expression while suppressing miR-383-5p expression. Knockdown of TMPO-AS1 reduced LPS-induced inflammatory responses and promoted proliferation and osteogenic differentiation of hPDLSCs, whereas overexpression of TMPO-AS1 produced opposite effects. Moreover, TMPO-AS1 directly targeted and bound miR-383-5p, exerting a negative regulatory effect. Reversal experiments demonstrated that inhibiting miR-383-5p significantly reversed the regulatory effects of TMPO-AS1 knockdown on inflammation and osteogenic differentiation, manifested as enhanced inflammatory response, suppressed cell proliferation, and reduced osteogenic differentiation capacity.

CONCLUSIONS

TMPO-AS1 promoted LPS-induced inflammatory responses and inhibited osteogenic differentiation of hPDLSCs by targeting and negatively regulating miR-383-5p, thereby contributing to the development and progression of CP.