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<p>Chronic periodontitis (CP) is a chronic infectious disease. Ubiquitin-specific protease 5 (USP5), a member of the deubiquitinase family, has garnered significant attention due to its crucial biological functions. In this study, we aimed to explore the function of USP5 in CP development. Human periodontal ligament mesenchymal stromal cells (hPDL-MSCs) were stimulated with LPS. qRT-PCR and western blot assay were performed to determine the expression of USP5, receptor-interacting protein kinase 1 (RIPK1), osteogenic markers, and macrophage polarization markers. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining assays were used to examine ALP activity and ARS quantification. Flow cytometry analysis was used to analyze cell apoptosis. Commercial kits were used to evaluated the levels of oxidative stress indicators. ELISA was performed for the concentrations of inflammatory factors. Co-immunoprecipitation (Co-IP) assay, GST pull-down assay and Ubiquitination assay were applied to analyze the relation between USP5 and RIPK1. USP5 was upregulated in the PDL tissues of CP patients and LPS-triggered hPDL-MSCs. Knockdown of USP5 contributed to the osteogenic differentiation of LPS-treated hPDL-MSCs and repressed the apoptosis, oxidative stress, inflammation, and M1-like macrophage polarization in LPS-treated hPDL-MSCs. Mechanically, USP5 was demonstrated to regulate RIPK1 expression through deubiquitination. Moreover, overexpression of RIPK1 restored the effects of USP5 knockdown on the osteogenic differentiation, apoptosis, oxidative stress injury, and macrophage polarization direction in LPS-treated hPDL-MSCs. USP5 deubiquitinated and stabilized RIPK1 to regulate the osteogenic differentiation, oxidative stress injury and macrophage polarization in CP.</p>

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USP5 inhibits osteogenic differentiation but promotes oxidative stress and M1-like macrophage polarization of human periodontal ligament stem cells via deubiquitinating and stabilizing RIPK1: insights from in vitro and in vivo analyses

  • 期刊论文

  • 发表日期：

    2026年7月6日

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  • Jinghong Mao,
  • Ming Qin

摘要

Chronic periodontitis (CP) is a chronic infectious disease. Ubiquitin-specific protease 5 (USP5), a member of the deubiquitinase family, has garnered significant attention due to its crucial biological functions. In this study, we aimed to explore the function of USP5 in CP development. Human periodontal ligament mesenchymal stromal cells (hPDL-MSCs) were stimulated with LPS. qRT-PCR and western blot assay were performed to determine the expression of USP5, receptor-interacting protein kinase 1 (RIPK1), osteogenic markers, and macrophage polarization markers. Alkaline phosphatase (ALP) and Alizarin red S (ARS) staining assays were used to examine ALP activity and ARS quantification. Flow cytometry analysis was used to analyze cell apoptosis. Commercial kits were used to evaluated the levels of oxidative stress indicators. ELISA was performed for the concentrations of inflammatory factors. Co-immunoprecipitation (Co-IP) assay, GST pull-down assay and Ubiquitination assay were applied to analyze the relation between USP5 and RIPK1. USP5 was upregulated in the PDL tissues of CP patients and LPS-triggered hPDL-MSCs. Knockdown of USP5 contributed to the osteogenic differentiation of LPS-treated hPDL-MSCs and repressed the apoptosis, oxidative stress, inflammation, and M1-like macrophage polarization in LPS-treated hPDL-MSCs. Mechanically, USP5 was demonstrated to regulate RIPK1 expression through deubiquitination. Moreover, overexpression of RIPK1 restored the effects of USP5 knockdown on the osteogenic differentiation, apoptosis, oxidative stress injury, and macrophage polarization direction in LPS-treated hPDL-MSCs. USP5 deubiquitinated and stabilized RIPK1 to regulate the osteogenic differentiation, oxidative stress injury and macrophage polarization in CP.