MicroRNA‐203 mediates Porphyromonas gingivalis LPS‐induced inflammation and differentiation of periodontal ligament cells

Abstract Aim In this study, we aimed to explore the effects of microRNA‐203 (miR‐203) on Porphyromonas gingivalis lipopolysaccharide ( P . g . LPS)‐stimulated periodontal ligament cells (PDLCs) and identify potential molecular targets for periodontitis treatment. Methods Periodontal ligament cells were stimulated by P . g . LPS, followed by quantification of miR‐203 and AP ‐ 1 expression. Next, loss‐ and gain‐of‐function experiments were applied in P . g . LPS‐induced PDLCs. The proliferation, apoptosis, and differentiation of PDLCs were determined, and mineralized nodule numbers were counted. Functional assays were used to identify interactions among miR‐203, activator protein ‐ 1 ( AP ‐ 1) , and intercellular adhesion molecule ‐ 1 ( ICAM ‐ 1 ). In addition, expression of osteogenesis‐related genes and release of proinflammatory factors were analyzed. Results miR‐203 was found to be downregulated while AP ‐ 1 was upregulated in PDLCs stimulated by P . g . LPS. The overexpression of miR‐203 promoted P . g . LPS‐stimulated PDLC proliferation and differentiation, inhibited apoptosis, and increased the number of mineralized nodules. miR‐203 was verified to downregulate AP ‐ 1 / ICAM ‐ 1 axis. miR‐203 overexpression reduced the secretion of proinflammatory factors while increasing the expression of osteogenesis‐related genes in P . g . LPS‐stimulated PDLCs, which was reversed by overexpressing AP ‐ 1 and ICAM ‐ 1 . Conclusion These experimental data demonstrated the potential inhibitory effects of overexpressed miR‐203 on periodontitis development by promoting PDLC differentiation and suppressing inflammatory responses through AP ‐ 1 / ICAM ‐ 1 axis.