首页> 外文期刊>Journal of Endodontics: Official Journal of American Association of Endodontists >The Role of Transient Receptor Potential Cation Channel, Subfamily C, Member 1 in the Odontoblast-like Differentiation of Human Dental Pulp Cells
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The Role of Transient Receptor Potential Cation Channel, Subfamily C, Member 1 in the Odontoblast-like Differentiation of Human Dental Pulp Cells

机译:瞬时受体潜在阳离子通道,亚家族C,构件1在人牙髓细胞的牙藤细胞样分化中的作用

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Introduction: Calcium 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. Methods: Immunohistochemical 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. Results: The 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. Conclusions: Our data indicated a pivotal role of TRPC1 in the odontoblastlike differentiation of hDPCs, which may be a therapeutic target to enhance reparative dentin formation.
机译:简介:通过促进人牙髓细胞(HDPC)的细胞增殖和分化,钙离子(CA2 +)积极参与重复的牙本质形成。瞬态受体潜在阳离子通道,亚家族C,构件1(TRPC1)在储存各种细胞类型的耗尽时激活CA2 +进入。但是,尚未报告TRPC1在HDPC中的功能。因此,我们旨在分析TRPC1在遭受异常形状的分化的HDPC中的作用。方法:使用免疫组织化学染色来确定纸浆组织中TRPC1的分布。 Western印迹分析用于检测HDPC的异常细胞状分化中TRPC1的蛋白质水平。用腺病毒载体进行TRPC1的敲低,以评估TRPC1在异常状的分化期间TRPC1在HDPC中的作用。结果:结果表明,TRPC1在牙科纸浆细胞的细胞质中高度表达,尤其是在健康纸浆的幼儿细胞层中。此外,TRPC1的蛋白质水平在HDPC的异常状分化期间以时间依赖性方式增加。重要的是,TRPC1的敲低,衰减了异藤细胞样分化的过程,如矿化结节的还原和牙本质唾液酸磷蛋白和牙本质基质蛋白的下调。此外,TRPC1的敲低降低了CA2 +进入HDPC的细胞质。结论:我们的数据表明TRPC1在HDPCs的Odontoblastlike分化中的枢转作用,其可以是增强牙本质形成的治疗靶标。

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