Format

Send to

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

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

Author information

1
Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China.
2
Department of Stomatology, Hospital Affiliated to Binzhou Medical University, Binzhou, Shandong, China.
3
Faculty of Dentistry, The University of Hong Kong, Hong Kong, China.
4
Shanghai Engineering Research Center of Tooth Restoration and Regeneration, Shanghai, China. qizhang@tongji.edu.cn.
5
Department of Endodontics, School of Stomatology, Tongji University, Shanghai, China. qizhang@tongji.edu.cn.

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

PMID:
30066216
DOI:
10.1007/s10735-018-9788-x
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center