El Karim Ikhlas A, McCrudden Maelíosa T C, McGahon Mary K, Curtis Tim M, Jeanneau Charlotte, Giraud Thomas, Irwin Chris R, Linden Gerard J, Lundy Fionnuala T, About Imad
School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, Northern Ireland.
Aix Marseille Université, CNRS, Institut des Sciences du Mouvement, Marseille, France.
J Endod. 2016 Apr;42(4):589-95. doi: 10.1016/j.joen.2015.12.017. Epub 2016 Feb 11.
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.
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.
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.
In conclusion, this study showed TRPA1 to be modulated by caries-induced inflammation and that Biodentine reduced TRPA1 expression and functional responses.
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，其中TRPA1在伤害感受和神经源性炎症中起核心作用。TRP通道的功能已被证明受炎症细胞因子调节。本研究的目的是调查炎症对成牙本质细胞TRPA1表达的影响，并确定生物活性玻璃离子水门汀（法国巴黎Septodent公司）对炎症诱导的TRPA1表达的影响。
采用免疫组织化学方法研究健康和龋损人牙髓组织中TRPA1的表达。在2 mmol/Lβ-甘油磷酸存在的情况下，将牙髓细胞分化为成牙本质样细胞，并将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。
免疫荧光染色显示TRPA1在成牙本质细胞胞体和成牙本质细胞突起中表达，在龋损牙齿中比健康牙齿中更强烈。肿瘤坏死因子α可诱导培养的成牙本质样细胞中TRPA1基因表达，而在生物活性玻璃离子水门汀存在的情况下，这种表达显著降低。钙微量荧光测定法和膜片钳记录显示了TRPA1通道的功能，我们的结果表明，生物活性玻璃离子水门汀处理后，肿瘤坏死因子α诱导的TRPA1反应显著降低。
总之，本研究表明TRPA1受龋齿诱导的炎症调节，生物活性玻璃离子水门汀可降低TRPA1表达和功能反应。
