miR‐27a‐5p alleviates periodontal inflammation by targeting phosphatase and tensin homolog deleted on chromosome ten

Introduction 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. Methods 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. Results 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. Conclusions miR‐27a‐5p alleviated the inflammatory response in periodontitis by targeting PTEN. This work declares that miR‐27a‐5p alleviates periodontal inflammation by targeting phosphatase and tensin homolog deleted on chromosome ten in ligatured‐induced periodontitis mice and macrophages stimulated with Porphyromonas gingivalis lipopolysaccharide, which contributes to further exploration in the pathogenesis of periodontitis.