During dentin formation, odontoblast polarization ensures that odontoblasts directionally secrete dentin matrix protein, leading to tubular dentin formation; however, little is known about the major features and regulatory mechanisms of odontoblast polarization. In a study of epithelial cell polarization, β-catenin was shown to serve as a structural component of cadherin-based adherens junctions to initiate cell polarity. However, the role of β-catenin in odontoblast polarization has not been well investigated. In this study, we explored whether β-catenin participated in odontoblast polarization to regulate the secretion of mineralization proteins. We established Col1-CreErt2; β-catenin exon3^fl/fl (CA-β-catenin) mice, which constitutively activate β-catenin in odontoblasts. CA-β-catenin mice exhibited disorganization and depolarization of incisor odontoblasts. Moreover, the incisor dentin was hypomineralized, and ectopic calcification was found in mouse incisor pulp. In addition, by constitutive activation of β-catenin, the expression levels of the core polarity molecule Cdc42 and its downstream polarity protein complex Par3-Par6-aPKC were decreased in the incisors of CA-β-catenin mice. These findings suggest that β-catenin plays an essential role in dentin formation by regulating odontoblast polarization.

在牙本质形成过程中，成牙本质细胞极化确保成牙本质细胞定向分泌牙本质基质蛋白，导致管状牙本质形成；然而，对成牙本质细胞极化的主要特征和调节机制知之甚少。在上皮细胞极化的研究中，β-连环蛋白被证明作为基于钙粘蛋白的粘附连接的结构成分来启动细胞极性。然而，β-连环蛋白在成牙本质细胞极化中的作用尚未得到很好的研究。在这项研究中，我们探讨了 β-连环蛋白是否参与了成牙本质细胞极化以调节矿化蛋白的分泌。我们建立了 Col1-CreErt2；β-连环蛋白外显子3 ^fl/fl(CA-β-catenin) 小鼠，组成性激活成牙本质细胞中的 β-catenin。CA-β-catenin 小鼠表现出切牙成牙本质细胞的解体和去极化。此外，门牙牙本质矿化不足，在小鼠门牙髓中发现异位钙化。此外，通过β-连环蛋白的组成型激活，核心极性分子Cdc42及其下游极性蛋白复合物Par3-Par6-aPKC在CA-β-连环蛋白小鼠门牙中的表达水平降低。这些发现表明β-连环蛋白通过调节成牙本质细胞极化在牙本质形成中起重要作用。