The Role of Transient Receptor Potential Cation Channel, Subfamily C, Member 1 in the Odontoblast-like Differentiation of Human Dental Pulp Cells.
The Role of Transient Receptor Potential Cation Channel, Subfamily C, Member 1 in the Odontoblast-like Differentiation of Human Dental Pulp Cells.
复制标题
瞬时受体电位阳离子通道，C 亚科，成员 1 在人牙髓细胞成牙本质细胞样分化中的作用。
DOI：
10.1016/j.joen.2016.10.021
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发表时间：
2017
影响因子：
4.2
通讯作者：
Lin Zhengmei
中科院分区：
文献类型：
--
作者：
Song Zhi;Chen Lingling;Guo Jia;Qin Wei;Wang Runfu;Huang Shuheng;Yang Xiaoting;Tian Yaguang;Lin Zhengmei
钙离子（Ca2+）通过促进人牙髓细胞（human dental pulp cells，hDPC）的增殖和分化，积极参与修复性牙本质的形成。瞬时受体电位阳离子通道，亚家族C，成员1（TRPC 1）在多种细胞类型中在钙池耗尽时激活Ca 2+内流。然而，TRPC 1在hDPC中的功能尚未报道。因此，我们的目的是分析TRPC 1在hDPC进行成牙本质细胞样分化的作用。MethodsImmunohistochemistry染色用于确定TRPC 1在牙髓组织中的分布。Western blot检测TRPC 1在hDPC向成牙本质细胞样分化过程中的蛋白表达水平。用腺病毒载体敲除TRPC 1，以评估TRPC 1在hDPC中的作用，在成牙本质细胞样分化过程中。结果表明，TRPC 1在牙髓细胞的细胞质中高度表达，特别是在健康牙髓的成牙本质细胞层。此外，TRPC 1蛋白水平增加，在成牙本质细胞样分化的hDPC的时间依赖性的方式。重要的是，TRPC 1的敲低减弱了成牙本质细胞样分化的过程，如矿化结节的减少和牙本质涎磷蛋白和牙本质基质蛋白1的下调所示。此外，TRPC 1的敲低降低了Ca2+进入hDPC的细胞质中。ConclusionsOur data indicated a potential role of TRPC 1 in the odontoblastlike differentiation of hDPC，这可能是一个治疗靶点，以提高修复性牙本质的形成。
IntroductionCalcium ions (Ca2+) actively participate in reparative dentin formation by promoting cellular proliferation and differentiation of human dental pulp cells (hDPCs). Transient receptor potential cation channel, subfamily C, member 1 (TRPC1) activates Ca2+entry upon store depletion in a variety of cell types. However, the function of TRPC1 in hDPCs has not been reported. Therefore, we aimed to analyze the role of TRPC1 in hDPCs undergoing odontoblast-like differentiation.MethodsImmunohistochemical staining was used to determine the distribution of TRPC1 in pulp tissues. Western blot analysis was used to detect the protein level of TRPC1 in the odontoblast-like differentiation of hDPCs. Knockdown of TRPC1 was performed with an adenoviral vector to evaluate the role of TRPC1 in hDPCs during odontoblast-like differentiation.ResultsThe results showed that TRPC1 was highly expressed in the cytoplasm of dental pulp cells, especially in the odontoblast layer of the healthy pulp. Moreover, the protein level of TRPC1 increased in a time-dependent manner during the odontoblast-like differentiation of hDPCs. Importantly, knockdown of TRPC1 attenuated the process of odontoblast-like differentiation as indicated by the reduction in mineralized nodules and the down-regulation of dentin sialophosphoprotein and dentin matrix protein 1. Moreover, knockdown of TRPC1 decreased Ca2+entry to the cytoplasm of hDPCs.ConclusionsOur data indicated a pivotal role of TRPC1 in the odontoblastlike differentiation of hDPCs, which may be a therapeutic target to enhance reparative dentin formation.