Scholarlink

<p>Pulpitis, a prevalent inflammatory dental disease, is characterized by persistent inflammation that severely compromises patients’ quality of life. While circular RNAs (circRNAs) have been established as key regulators in numerous pathological conditions, their functional significance in pulpitis remains poorly understood. In this study, we investigated the role of circ_0043582 using an in vitro lipopolysaccharide (LPS)-induced pulpitis cell model. Different concentrations of LPS were used to induce inflammation in human dental pulp cells (HDPCs) to stimulate an in vitro model of pulpitis. Circ_0043582, microRNA-940 (miR-940), and tumor necrosis factor receptor-associated factor (TRAF) 3 levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The impacts on cell functions were evaluated by detecting cell proliferation, apoptosis, inflammation, and oxidative stress. HDPCs were incubated with THP-1 cell supernatant, and M1 macrophage polarization was assessed by flow cytometry. Bioinformatic analysis using CircInteractome and miRDB predicted binding interactions between miR-940 and circ_0043582 or TRAF3, which were validated by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0043582 and TRAF3 were highly expressed in pulpitis patients and LPS-treated HDPCs, and miR-940 was decreased. Furthermore, circ_0043582 knockdown alleviated LPS-triggered proliferation inhibition, and apoptosis, inflammation, oxidative stress, and M1 polarization promotion in HDPCs. Mechanistically, circ_0043582 was identified as a sponge for miR-940, thereby regulating TRAF3 expression. Furthermore, LPS might activate the nuclear factor kappa-B (NF-κB) signaling pathway by regulating the circ_0043582/miR-940/TRAF3 axis in HDPCs. Our findings demonstrate that circ_0043582 knockdown attenuates LPS-mediated inflammatory damage in HDPCs by disrupting the miR-940/TRAF3/NF-κB signaling pathway, revealing a novel therapeutic avenue for pulpitis intervention.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Circ_0043582 promotes dental pulp cell injury via miR-940/TRAF3/NF-κB axis in pulpitis

  • 期刊论文

  • 发表日期：

    2025年12月17日

查看全文
  • Bin Wu,
  • Linlin Jiang,
  • Ying Mu

摘要

Pulpitis, a prevalent inflammatory dental disease, is characterized by persistent inflammation that severely compromises patients’ quality of life. While circular RNAs (circRNAs) have been established as key regulators in numerous pathological conditions, their functional significance in pulpitis remains poorly understood. In this study, we investigated the role of circ_0043582 using an in vitro lipopolysaccharide (LPS)-induced pulpitis cell model. Different concentrations of LPS were used to induce inflammation in human dental pulp cells (HDPCs) to stimulate an in vitro model of pulpitis. Circ_0043582, microRNA-940 (miR-940), and tumor necrosis factor receptor-associated factor (TRAF) 3 levels were detected by real-time quantitative polymerase chain reaction (RT-qPCR). The impacts on cell functions were evaluated by detecting cell proliferation, apoptosis, inflammation, and oxidative stress. HDPCs were incubated with THP-1 cell supernatant, and M1 macrophage polarization was assessed by flow cytometry. Bioinformatic analysis using CircInteractome and miRDB predicted binding interactions between miR-940 and circ_0043582 or TRAF3, which were validated by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Circ_0043582 and TRAF3 were highly expressed in pulpitis patients and LPS-treated HDPCs, and miR-940 was decreased. Furthermore, circ_0043582 knockdown alleviated LPS-triggered proliferation inhibition, and apoptosis, inflammation, oxidative stress, and M1 polarization promotion in HDPCs. Mechanistically, circ_0043582 was identified as a sponge for miR-940, thereby regulating TRAF3 expression. Furthermore, LPS might activate the nuclear factor kappa-B (NF-κB) signaling pathway by regulating the circ_0043582/miR-940/TRAF3 axis in HDPCs. Our findings demonstrate that circ_0043582 knockdown attenuates LPS-mediated inflammatory damage in HDPCs by disrupting the miR-940/TRAF3/NF-κB signaling pathway, revealing a novel therapeutic avenue for pulpitis intervention.