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      Wnt Signaling Activation in Gingival Epithelial Cells and Macrophages of Experimental Periodontitis.

      1 , 1
      Dentistry journal
      MDPI AG
      Wnt signaling, macrophage, periodontitis

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          Abstract

          Objective: Wingless/integrated (Wnt) signaling plays critical roles in maintaining environmental homeostasis and is also involved in the pathogenesis of inflammatory diseases. However, its role in macrophages during periodontitis is not well understood. The present study aims to investigate the interaction between Wnt signaling and macrophages in the context of periodontitis. Methods: Experimental periodontitis was induced in C57/BL6 mice using a Porphyromonas gingivalis (P.g)-associated ligature for 14 days. Immunohistochemistry was performed to study the expression of the pro-inflammatory cytokine tumor necrosis factor (TNF-α), the stabilization of β-catenin, and the macrophage marker F4/80 in the periodontal tissues. The effect of Wnt signaling on TNF-α was examined using Western blot analysis in Raw 264.7 murine macrophages stimulated by Wnt3a-conditioned medium, with or without Wnt3a antibody neutralization, and compared with primary cultured gingival epithelial cells (GECs). The effect of P.g lipopolysaccharide (LPS) on Wnt signaling was assessed by analyzing key components of the Wnt signaling pathway, including the activity of low-density lipoprotein receptor-related protein (LRP) 6 and nuclear accumulation of β-catenin in GEC and Raw 264.7 cells. Results: Over-expressions of TNF-α and activated β-catenin were presented in the macrophages in the gingiva from mice with P.g-associated ligature-induced periodontitis. The expression patterns of TNF-α and activated β-catenin were consistent with the expression of F4/80. In Raw 264.7 cells, activation of the Wnt signaling pathway led to an increase in TNF-α, but this effect was not observed in GEC. Additionally, treatment with LPS induced β-catenin accumulation and LRP6 activation in Raw 264.7 cells, which were blocked by the addition of Dickkopf-1(DKK1). Conclusions: Wnt signaling was aberrantly activated in the macrophages in experimental periodontitis. The activation of Wnt signaling in the macrophages may play a pro-inflammatory role in periodontitis. Targeting specific signaling pathways, such as the Wnt pathway, may hold promise for developing novel therapeutic interventions for periodontitis.

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          Author and article information

          Journal
          Dent J (Basel)
          Dentistry journal
          MDPI AG
          2304-6767
          2304-6767
          May 09 2023
          : 11
          : 5
          Affiliations
          [1 ] Department of Immunology and Infectious Diseases, The Forsyth Institute, 245 First Street, Cambridge, MA 02142, USA.
          Article
          dj11050129
          10.3390/dj11050129
          10217294
          37232780
          60d86e01-4f8f-45b5-8c50-5aaafd269676
          History

          periodontitis,Wnt signaling,macrophage
          periodontitis, Wnt signaling, macrophage

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