Department of Oral Physiology, BK21 PLUS Project, School of Dentistry, Pusan National University, Yangsan, South Korea.
Department of Orthodontics, BK21 PLUS Project, School of Dentistry, Pusan National University, Yangsan, South Korea.
J Endod. 2018 Dec;44(12):1826-1831. doi: 10.1016/j.joen.2018.08.003.
Pentraxin 3 (PTX3) has been suggested as a novel inflammatory biomarker in inflammation-associated diseases. The aim of this study was to examine the role of PTX3 in the inflammatory response of human dental pulp cells (HDPCs).
HDPCs were treated with tumor necrosis factor alpha (TNF-α), and total RNA and protein were extracted. PTX3 messenger RNA and protein expression levels were analyzed using reverse transcription polymerase chain reaction and Western blotting, respectively. For PTX3 knockdown, HDPCs were transfected with a small interfering RNA against human PTX3. Macrophage chemotaxis after PTX3 silencing in HDPCs was assessed by transwell migration assays.
TNF-α increased PTX3 messenger RNA and protein levels in HDPCs. TNF-α-induced PTX3 expression was mediated by extracellular signal-regulated kinase 1/2 and nuclear factor kappa B. PTX3 knockdown decreased the expression levels of interleukin 6, interleukin 8, and monocyte chemoattractant protein 1 after stimulation with TNF-α in HDPCs. Moreover, PTX3 silencing in HDPCs significantly decreased the chemotactic migration of macrophages.
Our findings indicate PTX3 plays a critical role in the regulation of pulp inflammatory processes and reveal its underlying molecular mechanism.
Pentraxin 3（PTX3）被认为是与炎症相关疾病的新型炎症生物标志物。本研究旨在探讨 PTX3 在人牙髓细胞（HDPCs）炎症反应中的作用。
用肿瘤坏死因子-α（TNF-α）处理 HDPCs，提取总 RNA 和蛋白质。采用逆转录聚合酶链反应和 Western blot 分别分析 PTX3 信使 RNA 和蛋白表达水平。为了进行 PTX3 敲低，用针对人 PTX3 的小干扰 RNA 转染 HDPCs。通过 Transwell 迁移实验评估 PTX3 沉默后 HDPCs 中巨噬细胞的趋化性。
TNF-α增加了 HDPCs 中的 PTX3 信使 RNA 和蛋白水平。TNF-α 诱导的 PTX3 表达是通过细胞外信号调节激酶 1/2 和核因子 kappa B 介导的。PTX3 敲低后，HDPCs 中 TNF-α 刺激后白细胞介素 6、白细胞介素 8 和单核细胞趋化蛋白 1 的表达水平降低。此外，PTX3 沉默显著降低了 HDPCs 中巨噬细胞的趋化迁移。
我们的研究结果表明，PTX3 在牙髓炎症过程的调控中起着关键作用，并揭示了其潜在的分子机制。
