细胞外信号调节激酶信号转导通路在牙发生和再生中的作用

Extracellular signal-regulated kinase signal transduction pathway in dentification and tooth regeneration

细胞外信号调节激酶(ERK)信号转导通路广泛调控牙发生及其形态发育,且其作用伴随在牙发生的各个时期。成纤维细胞生长因子-10通过激活牙上皮细胞中的ERK信号转导通路促进牙胚发生发育。在间质细胞的牙向分化以及牙周组织的发生和分化过程中,ERK信号转导通路皆起着重要的作用。三氧化聚合物可通过磷酸化激活ERK,从而诱导牙质细胞分化。ERK信号转导通路对于牙髓干细胞(DPSC)向成牙质细胞的分化很重要,激活DPSC中的ERK信号转导通路对成牙质细胞的再生是一条有效途径。在牙发生过程中,机械压力可诱导间质细胞向成骨细胞分化;反之,机械拉力则通过增强ERK磷酸化促进DPSC增殖,抑制其向成骨细胞分化。ERK信号转导通路既有利于DPSC迁移,也有利于牙髓组织重建。本文就ERK信号转导通路在牙发生过程中的作用作一综述,以探讨其对牙再生的影响。

Extracellular signal-regulated kinase（ERK） is an important signaling transduction pathway involved in tooth development. The pathway widely regulates dentification and tooth morphogenesis in each developmental stage. Fibroblast growth factor-10 promotes the initiation and development of tooth germ by activating the ERK signaling transduction pathway in dental epithelium. The pathway also regulates the differentiation of mesenchymal stem cells into odontoblasts and the initiation and differentiation of periodontium. Mineral trioxide aggregate can induce odontoblast differentiation by phosphorylating and activating ERK. The pathway is critical in inducing the differentiation of dental pulp stem cell（DPSC） into odontoblasts; hence, activating the ERK signaling pathway in DPSC may be an effective way to regenerate odontoblasts. Hydrostatic pressures during dentification promote mesenchymal osteodifferentiation. By contrast, mechanical stretch inhibits osteogenic differentiation by increasing pERK-mediated cell proliferation. The ERK signaling pathway facilitates the migration of DPSC and the regeneration of dental pulp tissue. This review enumerates the fimctions of the ERK pathway in dentification and discusses how ERK influences tooth regeneration.