# The expression profile and clinical relevance of miR-125a-5p in individuals with chronic periodontitis

## TL;DR

This study explores how miR-125a-5p is linked to chronic periodontitis and its potential as a treatment target.

## Contribution

The study identifies miR-125a-5p as a novel regulator of periodontal inflammation through its target BTG2.

## Key findings

- miR-125a-5p levels are higher in patients with chronic periodontitis and correlate with disease severity.
- miR-125a-5p promotes inflammation and oxidative stress in periodontal ligament fibroblasts.
- BTG2 is confirmed as a direct target of miR-125a-5p, mediating its effects on cell function.

## Abstract

Chronic periodontitis is a prevalent inflammatory disease, and miR-125a-5p’s role in its pathogenesis remains unclear.

We examined the clinical significance and mechanisms of miR-125a-5p in chronic periodontitis by testing two hypotheses: (1) miR-125a-5p expression is altered in chronic periodontitis and correlates with clinical indicators; (2) miR-125a-5p regulates periodontal ligament fibroblast (PDLF) functions by targeting specific genes, contributing to disease pathogenesis.

Pearson correlation analysis assessed the association between miR-125a-5p expression and key clinical indicators. Receiver operating characteristic (ROC) curve analysis evaluated its diagnostic performance in chronic periodontitis. Periodontal ligament fibroblasts were treated with lipopolysaccharide (LPS) to establish an inflammatory model. miR-125a-5p and B-cell translocation gene 2 (BTG2) expression levels were measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell count kit-8 (CCK-8) assay and enzyme-linked immunosorbent assay (ELISA) assessed miR-125a-5p’s effects on cell proliferation, oxidative stress, and inflammation. The direct interaction between miR-125a-5p and BTG2 was confirmed using a dual-luciferase reporter assay.

The expression level of miR-125a-5p in the gingival crevicular fluid of patients with chronic periodontitis was significantly upregulated and positively correlated with the severity of periodontal tissue damage. In the LPS-induced PDLFs model, miR-125a-5p expression was upregulated, cell proliferation capacity was suppressed, oxidative stress was induced, and levels of inflammation-related factors were increased. Notably, transfection with a miR-125a-5p inhibitor effectively reversed these effects. Moreover, the study confirmed that BTG2 is a direct target gene of miR-125a-5p, and that miR-125a-5p exerts its regulatory effects on cellular functions through targeting BTG2.

miR-125a-5p is potentially associated with chronic periodontitis, and may serve as a therapeutic target.