Lncrna-Kat7/Gpx4 Axis Inhibit Ferroptosis In Periodontal Ligament Fibroblasts.

Periodontitis, as a common clinical oral disease, has been confirmed to be closely related to ferroptosis, what’s more, studies have shown that Long non-coding RNA (LncRNA) plays an important role in ferroptosis of periodontitis as well, which provides ideas for us to explore the internal relationship between LncRNA-KAT7, ferroptosis and periodontitis. In this study, Lipopolysaccharide (LPS) was used to stimulate Human periodontal ligament fibroblasts (hPDLFs) to establish an in vitro experimental periodontitis cell model. Transmission electron microscopy was used to discribe the cellular substructure. DCFH-DA probe was used to detect the level of ROS. CCK-8 was used to detect the level of cell death. qRT-PCR and Western blot were used to detect the expression levels of mRNA and protein. MiRBase and TargetScan were used to predict the potential binding sites between LncRNA-KAT7 and GPX4. Dual luciferase reporter gene was used to verify the binding between LncRNA-KAT7, GPX4 and miR-92a-2-5p. 1. LncRNA-KAT7 and GPX4 were lowly expressed in LPS-stimulated hPDLFs. 2. Overexpression of LncRNA-KAT7 could inhibit the cell death and ROS level of LPS-induced hPDLFs, and promote the expression of ferroptosis-related proteins GPX4, SLC7A11 and HO-1, on the contrary, knockdown of LncRNA-KAT7 turns out opposite results. 3. LncRNA-KAT7 and GPX4 could target and bind to miR-92a-2-5p, furthermore, LncRNA-KAT7 has an axial effect on GPX4. LncRNA-KAT7/GPX4 axis may affect the progression of periodontitis by regulating ferroptosis.