Sheng Xinyue, Li Jingzhou, Ma Haozhen, He Hongwen, Liu Qin, Jia Shilin, Zhang Fuping, Huang Fang
Hospital of Stomatology, Sun Yat-sen University, Guangzhou 510055, China.
Guangdong Provincial Key Laboratory of Stomatology, Guangzhou 510080, China.
Biomolecules. 2025 Feb 20;15(3):316. doi: 10.3390/biom15030316.
This study explored the role of Piezo1 in the odontogenic differentiation of dental papilla cells (DPCs) and tissue, focusing on a mechanism involving family with sequence similarity 83, member G (FAM83G). Here, we found Piezo1, a mechanosensitive cation channel, was upregulated during odontogenesis in DPCs and dental papilla tissues. Knockdown of Piezo1 impaired odontogenic differentiation, while its activation by Yoda1 enhanced the process. Using a 3D culture model and an ectopic transplantation model, we confirmed Piezo1's role in vivo. RNA sequencing (RNA-seq) analysis revealed that FAM83G was upregulated in Piezo1-knockdown cells, and FAM83G silencing enhanced odontogenesis in DPCs. These findings indicate that Piezo1 positively regulates odontogenesis by inhibiting FAM83G in DPCs both in vitro and in vivo, with Piezo1 representing a potential target for dental tissue regeneration.
本研究探讨了Piezo1在牙乳头细胞(DPCs)和成牙组织的牙源性分化中的作用,重点关注涉及序列相似性家族83成员G(FAM83G)的机制。在此,我们发现机械敏感阳离子通道Piezo1在DPCs和成牙组织的牙发生过程中上调。Piezo1的敲低会损害牙源性分化,而Yoda1对其激活则会增强这一过程。使用三维培养模型和异位移植模型,我们在体内证实了Piezo1的作用。RNA测序(RNA-seq)分析显示,FAM83G在Piezo1敲低的细胞中上调,而FAM83G的沉默增强了DPCs的牙发生。这些发现表明,Piezo1在体外和体内均通过抑制DPCs中的FAM83G来正向调节牙发生,Piezo1代表了牙组织再生的一个潜在靶点。