ArticleMolecular biology reports2026
Mechanism study of METTL3 regulating Wnt/β-Catenin signalling in Pg.LPS-stimulated hSCAPs odontogenic differentiation.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background Apical periodontitis (AP) is one of the most common infectious diseases in dental clinics; the success of root canal treatment is largely limited by the severity of bone destruction, residual infection, and ongoing inflammation. Stem cells from the apical papilla (SCAPs) can promote periapical bone repair and improve the outcomes of root canal treatment. Existing studies suggest that inflammatory environments can affect the differentiation potential of SCAPs, but the underlying molecular mechanisms are still unclear. Methods and Results In this study, we isolated, cultured, and characterized SCAPs from six immature permanent teeth extracted from five subjects for orthodontic treatment or tooth impaction. After 7 and 14 days of LPS-induced mineralization, qPCR and Western blot results showed that dentin matrix acidic phosphoprotein (DMP) expression was significantly upregulated, while METTL3, β-catenin, and dentin sialophosphoprotein (DSPP) expression were significantly downregulated. Alizarin Red staining showed reduced formation of mineralized nodules. Lentivirus-mediated overexpression of METTL3 (Lv-M) in LPS-treated SCAPs significantly increased β-catenin, DMP, and DSPP levels on the 7th and 14th days of mineralization induction, confirmed by qPCR and Western blot. Alkaline phosphatase (ALP) and Alizarin Red staining showed a clear increase in mineralized nodules. Using in combination with Wnt inhibitor Dickkopf-related protein 1 (DKK-1) significantly reversed these promoting effects (P < 0.05). Conclusion The study confirms that under inflammatory conditions, METTL3 positively regulates odontogenic differentiation of human SCAPs by activating the Wnt/β-catenin pathway. These findings provide theoretical support for exploration of the regulatory network of stem cell regeneration and differentiation inflammatory microenvironments.
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