Modulation of autophagy and inflammation in human periodontal ligament fibroblasts by the LncRNA-KAT7/miR-455-5p/NRG1 axis in response to LPS.

Autophagy plays a pivotal role in the development of periodontitis, and long non-coding RNA (lncRNA) significantly influences the regulation of autophagy during the progression of this disease. However, the precise regulatory mechanisms remain elusive. Our prior research indicated that lncRNA-KAT7 is critically involved in periodontitis development, yet the specific molecular mechanisms by which lncRNA-KAT7 impacts periodontitis are still undefined. In this study, we discovered that both lncRNA-KAT7 and Neuroregulin-1 (NRG1) are downregulated in periodontitis. Alterations in lncRNA-KAT7 levels lead to corresponding changes in NRG1. Furthermore, the overexpression of lncRNA-KAT7 and NRG1 enhances cellular autophagy, diminishes the production of inflammatory cytokines (IL-6, IL-17, TNF), and reduces cell apoptosis. In contrast, the suppression of lncRNA-KAT7 yields opposite effects. Delving into the molecular mechanism, we confirmed that miR-455-5p interacts with both lncRNA-KAT7 and NRG1. The silencing of lncRNA-KAT7 is accompanied by changes in cell autophagy, cell apoptosis, and alterations in inflammatory cytokines, which can be mitigated by the overexpression of miR-455-5p. In conclusion, this study demonstrates that lncRNA-KAT7 is involved in autophagy-mediated apoptosis and the inflammatory response in LPS-stimulated Human Periodontal Ligament Fibroblasts (hPDLFs) via the miR-455-5p/NRG1 axis, offering a novel therapeutic avenue for periodontitis treatment.