MicroRNA-5011-5p attenuates LPS-induced inflammatory damage in periodontal ligament cells by targeting KLF6: an in vitro study.

Periodontitis is a long-term inflammatory condition that leads to the breakdown of the structures supporting the teeth and loss of bone. MicroRNAs are important regulators in controlling inflammation and maintaining tissue balance. This study explores the function of miR-5011-5p in periodontal ligament cells (PDLCs) under lipopolysaccharide (LPS)-induced inflammatory stress. It investigates its regulatory relationship with KLF6, a transcription factor implicated in inflammation and apoptosis. In periodontal ligament cells stimulated with LPS, the expression of miR-5011-5p decreased, accompanied by a notable increase in KLF6 and pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6. Functional assays revealed that overexpression of miR-5011-5p suppressed cytokine production, promoted cell viability, and reduced apoptosis. Conversely, reintroduction of KLF6 reversed these protective effects. Experiments using dual-luciferase reporter assays verified that KLF6 is a direct target regulated by miR-5011-5p. Additionally, Western blot results demonstrated that miR-5011-5p increased the levels of the anti-apoptotic protein Bcl-2 while decreasing the pro-apoptotic protein Bax, effects that were reversed when KLF6 was overexpressed. These findings suggest that miR-5011-5p mitigates LPS-induced periodontal inflammation and apoptosis by suppressing KLF6 expression. The miR-5011-5p and KLF6 interaction pathway could serve as a novel molecular target for developing therapies to treat periodontitis.