Constitutive activation of β-catenin in ameloblasts leads to incisor enamel hypomineralization

J Mol Histol. 2018 Oct;49(5):499-507. doi: 10.1007/s10735-018-9788-x. Epub 2018 Jul 31.

Abstract

Enamel is the hardest tissue with the highest degree of mineralization protecting the dental pulp from injury in vertebrates. The ameloblasts differentiated from ectoderm-derived epithelial cells are a single cell layer and are important for the enamel formation and mineralization. Wnt/β-catenin signaling has been proven to exert an important role in the mineralization of bone, dentin and cementum. Little was known about the regulatory mechanism of Wnt/β-catenin signaling pathway in ameloblasts during amelogenesis, especially in the mineralization of enamel. To investigate the role of β-catenin in ameloblasts, we established Amelx-Cre; β-catenin∆ex3fl/fl (CA-β-catenin) mice, which could constitutive activate β-catenin in ameloblasts. It showed the delayed mineralization and eventual hypomineralization in the incisor enamel of CA-β-catenin mice. Meanwhile, the amelogenesis-related proteinases Mmp20 and Klk4 were decreased in the incisors of CA-β-catenin mice. These data indicated that β-catenin plays an essential role in differentiation and function of ameloblasts during amelogenesis.

Keywords: Ameloblast; Enamel; Hypomineralization; β-Catenin.

MeSH terms

  • Ameloblasts / metabolism*
  • Amelogenesis
  • Animals
  • Dental Enamel / chemistry*
  • Dental Enamel Hypoplasia / etiology*
  • Kallikreins / metabolism
  • Matrix Metalloproteinase 20 / metabolism
  • Mice
  • Wnt Signaling Pathway
  • beta Catenin / metabolism*

Substances

  • CTNNB1 protein, mouse
  • beta Catenin
  • Kallikreins
  • kallikrein 4
  • Matrix Metalloproteinase 20
  • Mmp20 protein, mouse