Publication date: Available online 12 September 2018
Source: Archives of Oral Biology
Author(s): Wenying Song, Yanli Wang, Qing Chu, Congcong Qi, Yuehua Gao, Yan Gao, Lili Xiang, Xu Zhenzhen, Yuguang Gao
Abstract
Objectives
In order to understand the specific in vivo function of transforming growth factor-beta1 (TGF-β1), we successfully established aTGF-β1 deficient mouse model using a conditional knockout method. In the present study, we aimed to further understand the potential role of TGF-β1 in enamel formation.
Design
Transgenic mice withoutTGF-β1 in epithelial cells were generated. Scanning electron microscopy and micro-computed tomography analysis were used to detect the dental appearance, enamel microstructure and tooth density. Histological analysis was used to examine the residual organic matrix of enamel. Quantitative real-time polymerase chain reaction was used to analyze the expressions of enamel matrix proteins at the mRNA level.
Results
The enamel of mandibular molars and incisors inTGF-β1 conditional knockout mice displayed severe attrition and lower density compared with the wild-type littermates. A slender microstructure of enamel rod was observed, and enamel matrix proteins were retained in the enamel space at the maturation stage in conditional knockout mice. Moreover, the expressions of enamel matrix protein-encoding genes, such as amelogenin (Amelx), ameloblastin (Ambn), Enamelin (Enam) and matrix metalloproteinase-20 (Mmp-20), were increased in enamel organs of conditional knockout mice. On the other hand, the expressions of Amelotin (Amtn), kallikrein-related peptidase-4 (Klk4), C4orf26 and WD repeat-containing protein 72 (Wdr72) were dramatically decreased at the transition and maturation stages.
Conclusions
TGF-β1 played an important role in enamel mineralization through decreasing synthesis ofAmelx, Ambn and Enam and increasing synthesis of Klk4, Amtn, Corf26 and Wdr72.
https://ift.tt/2CR946Z
Δεν υπάρχουν σχόλια:
Δημοσίευση σχολίου