MiR-27a-5p alleviates periodontal inflammation by targeting phosphatase and tensin homolog deleted on chromosome ten.

Abstract

MicroRNAs (miRNAs), a type of non-coding RNA, have been demonstrated to be essential posttranscriptional modulators in oral diseases and inflammatory responses. However, the specific role of miR-27a-5p in periodontitis requires further investigation. In this study, we used both cellular and animal models to determine how miR-27a-5p affects the pathogenesis of periodontitis and its associated biological functions. Quantitative real-time polymerase chain reaction and western blotting were used to analyze the expression of cytokines, phosphatase and tensin homolog deleted on chromosome ten (PTEN), and miR-27a-5p transcription. Investigation of alveolar bone resorption and inflammation of the periodontium in ligature-induced periodontitis in mice was performed using micro-computed tomography (micro-CT), hematoxylin-eosin (HE) staining, and tartrate-resistant acid phosphatase (TRAP) staining. The binding of miR-27a-5p and PTEN was predicted using the TargetScan database and experimentally confirmed using dual luciferase reporter gene assays. The inflamed gingiva showed lower levels of miR-27a-5p. Macrophages from miR-27a-5p-/- mice produced much higher quantities of pro-inflammatory cytokines owing to the stimulation of Porphyromonas gingivalis lipopolysaccharide, and miR-27a-5p-/- mice with ligature-induced periodontitis also exhibited more severe alveolar bone resorption and damage to the periodontium. Target validation assays identified PTEN as a direct target of bona. Blocking PTEN expression partially reduced inflammation, both in vitro and in vivo. miR-27a-5p alleviated the inflammatory response in periodontitis by targeting PTEN.