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<p>Periodontal ligament stem cells (PDLSCs) possess osteogenic differentiation potential. Inflammatory microenvironments impair PDLSC function under periodontitis. Vanin-1 (VNN1) is upregulated in periodontitis gingival tissues and correlates with disease severity. This study investigated the precise role of VNN1 in periodontitis pathogenesis. Human PDLSCs (hPDLSCs) were stimulated with lipopolysaccharide (LPS) to mimic an inflammatory model. Osteogenic differentiation was assessed by alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining. Expression analysis was performed by quantitative PCR and immunoblot analysis. ROS amount detection was conducted using an assay kit. IL-1β, IL-6, and TNF-α secretion levels were measured by ELISA. The binding of forkhead box A1 (FOXA1) to the VNN1 promoter region was predicted by the JASPAR tool and confirmed by chromatin immunoprecipitation (ChIP) assay. VNN1 and FOXA1 levels were increased in diseased gingival tissues of periodontitis patients and LPS-challenged hPDLSCs. Functionally, depletion of VNN1 attenuated inflammation and enhanced osteogenic differentiation in LPS-stimulated hPDLSCs. Mechanistically, FOXA1 positively regulated VNN1 expression by binding to the VNN1 promoter region. Moreover, VNN1 re-expression reversed the anti-inflammatory and pro-osteogenic effects of FOXA1 silencing in LPS-challenged hPDLSCs. Our study identifies the&#xa0;FOXA1–VNN1 axis&#xa0;as a novel regulator&#xa0;that links inflammation to impaired osteogenesis in hPDLSCs under LPS inflammatory conditions.</p>

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VNN1, upregulated by FOXA1, suppresses osteogenic differentiation and promotes inflammation in LPS-induced periodontal ligament stem cells

  • 期刊论文

  • 发表日期：

    2025年12月13日

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  • Xianglin Lin,
  • Qianhui Hu,
  • Chengzhong Wu,
  • Pengcheng Ye,
  • Xia Shao

摘要

Periodontal ligament stem cells (PDLSCs) possess osteogenic differentiation potential. Inflammatory microenvironments impair PDLSC function under periodontitis. Vanin-1 (VNN1) is upregulated in periodontitis gingival tissues and correlates with disease severity. This study investigated the precise role of VNN1 in periodontitis pathogenesis. Human PDLSCs (hPDLSCs) were stimulated with lipopolysaccharide (LPS) to mimic an inflammatory model. Osteogenic differentiation was assessed by alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining. Expression analysis was performed by quantitative PCR and immunoblot analysis. ROS amount detection was conducted using an assay kit. IL-1β, IL-6, and TNF-α secretion levels were measured by ELISA. The binding of forkhead box A1 (FOXA1) to the VNN1 promoter region was predicted by the JASPAR tool and confirmed by chromatin immunoprecipitation (ChIP) assay. VNN1 and FOXA1 levels were increased in diseased gingival tissues of periodontitis patients and LPS-challenged hPDLSCs. Functionally, depletion of VNN1 attenuated inflammation and enhanced osteogenic differentiation in LPS-stimulated hPDLSCs. Mechanistically, FOXA1 positively regulated VNN1 expression by binding to the VNN1 promoter region. Moreover, VNN1 re-expression reversed the anti-inflammatory and pro-osteogenic effects of FOXA1 silencing in LPS-challenged hPDLSCs. Our study identifies the FOXA1–VNN1 axis as a novel regulator that links inflammation to impaired osteogenesis in hPDLSCs under LPS inflammatory conditions.