Affiliation:
1. College of Stomatology Chongqing Medical University Chongqing China
2. Chongqing Municipal Key Laboratory of Oral Biomedical Engineering of Higher Education Chongqing Medical University Chongqing China
3. Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences Chongqing Medical University Chongqing China
4. Department of Laboratory Medicine Key Laboratory of Diagnostic Medicine (Ministry of Education) Chongqing Medical University Chongqing China
Abstract
AbstractObjectiveThis study aimed to investigate the effect of METTL3 knockdown on osteogenic differentiation of human periodontal ligament stem cells (PDLSCs) in the weak inflammation microenvironments, as well as the underlying mechanisms.Materials and MethodsPDLSCs were stimulated by lipopolysaccharide from Escherichia coli (E. coli LPS), followed by quantification of METTL3. METTL3 expression was assessed using RT‐qPCR and Western blot analysis in periodontitis. METTL3 knockdown PDLSCs were stimulated with or without E. coli LPS. The evaluation included proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules. Bioinformatics analysis and Western blot determined the association between METTL3 and the PI3K/Akt pathway.ResultsMETTL3 was overexpressed in periodontitis. METTL3 knockdown in PDLSCs reduced proinflammatory cytokines, osteogenic markers, ALP activity, and mineralized nodules in both environments. Bioinformatics analysis suggested a link between METTL3 and the PI3K/Akt pathway. METTL3 knockdown inhibited PI3K/Akt signaling pathway activation.ConclusionMETTL3 knockdown might inhibit osteogenesis in PDLSCs through the inactivation of PI3K/Akt signaling pathway. Concomitant findings might shed novel light on the roles and potential mechanisms of METTL3 in the LPS‐stimulated inflammatory microenvironments of PDLSCs.
Funder
National Natural Science Foundation of China
Subject
General Dentistry,Otorhinolaryngology