Biodentine Reduces Tumor Necrosis Factor Alpha-induced TRPA1 Expression in Odontoblastlike Cells

Biodentine Reduces Tumor Necrosis Factor Alpha-induced TRPA1 Expression in Odontoblastlike Cells
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DOI:
10.1016/j.joen.2015.12.017
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发表时间:
2016-04-01
影响因子:
4.2
通讯作者:
About, Imad
About, Imad
中科院分区:
医学2区
文献类型:
--
作者:
El Karim, Ikhlas A.;McCrudden, Maeliosa T. C.;About, Imad

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简介:瞬时受体电位 (TRP) 离子通道已成为神经元和非神经元细胞中重要的细胞传感器,TRPA1 在伤害感受和神经源性炎症中发挥着核心作用。 TRP 通道的功能已被证明受炎症细胞因子的调节。本研究的目的是研究炎症对成牙本质细胞 TRPA1 表达的影响,并确定 Biodentine(Septodent,巴黎,法国)对炎症诱导的 TRPA1 表达的影响。方法:采用免疫组织化学方法研究健康和龋齿牙髓组织中 TRPA1 的表达。在 2 mmol/L β-甘油磷酸存在下,牙髓细胞分化为成牙本质细胞样细胞,这些细胞用于定量聚合酶链反应、蛋白质印迹、钙成像和膜片钳研究。结果:免疫荧光染色显示。 TRPA1 在成牙本质细胞体和成牙本质细胞过程中表达,与健康牙齿相比,龋齿中的 TRPA1 表达更为强烈。 TRPA1 基因表达在培养的成牙本质细胞样细胞中被肿瘤坏死因子 α 诱导,并且在 Biodentine 存在下该表达显着降低。 TRPA1 通道的功能通过钙微荧光测定和膜片钳记录显示,我们的结果表明,Biodentine 治疗后肿瘤坏死因子 α 诱导的 TRPA1 反应显着减少。结论:总而言之,这项研究表明 TRPA1 受到龋齿诱导的炎症的调节,并且 Biodentine 降低了 TRPA1 的表达和功能反应。
Introduction: The transient receptor potential (TRP) ion channels have emerged as important cellular sensors in both neuronal and non-neuronal cells, with TRPA1 playing a central role in nociception and neurogenic inflammation. The functionality of TRP channels has been shown to be modulated by inflammatory cytokines. The aim of this study was to investigate the effect of inflammation on odontoblast TRPA1 expression and to determine the effect of Biodentine (Septodent, Paris, France) on inflammatory-induced TRPA1 expression. Methods: Immunohistochemistry was used to study TRPA1 expression in pulp tissue from healthy and carious human teeth. Pulp cells were differentiated to odontoblastlike cells in the presence of 2 mmol/L beta-glycerophosphate, and these cells were used in quantitative polymerase chain reaction, Western blotting, calcium imaging, and patch clamp studies. Results: Immunofluorescent staining revealed. TRPA1 expression in odontoblast cell bodies and odontoblast processes, which was more intense in carious versus healthy teeth. TRPA1 gene expression was induced in cultured odontoblastlike cells by tumor necrosis factor alpha, and this expression was significantly reduced in the presence of Biodentine. The functionality of the TRPA1 channel was shown by calcium microfluorimetry and patch clamp recording, and our results showed a significant reduction in tumor necrosis factor alpha induced TRPA1 responses after Biodentine treatment. Conclusions: In conclusion, this study showed TRPA1 to be modulated by caries-induced inflammation and that Biodentine reduced TRPA1 expression and functional responses.