Yokozeki Masahiko, Afanador Elaine, Nishi Masumi, Kaneko Kazuyuki, Shimokawa Hitoyata, Yokote Koutaro, Deng Chuxia, Tsuchida Kunihiro, Sugino Hiromu, Moriyama Keiji
Department of Orthodontics, School of Dentistry, The University of Tokushima, 3-18-15 Kuramoto-cho, Tokushima 770-8504, Japan.
Biochem Biophys Res Commun. 2003 Jun 6;305(3):684-90. doi: 10.1016/s0006-291x(03)00806-4.
Smad3 is an intracellular signaling molecule that mediates the signal from transforming growth factor-beta (TGF-beta) and activin receptors. In this study, we reveal hypomineralized enamel in mice with the targeted deletion of the Smad3 gene. The Smad3 (-/-) mice had chalky white incisor enamel, while the enamel of the wild-type or Smad3 (+/-) mice was yellow-brown. Histological analysis of the undecalcified sections showed that the enamel thickness of the maxillary incisors in the Smad3 (-/-) mice was similar to that of the wild-type and Smad3 (+/-) mice while that the enamel of the maxillary molars in Smad3 (-/-) mice was disrupted in places. Microcomputed tomography (microCT) analysis revealed that the mineralization of the maxillary incisors and mandibular molars in the Smad3 (-/-) mice showed significant reduction in the degree of mineralization when compared to that of the wild-type and Smad3 (+/-) mice. Scanning electron microscopic (SEM) analysis of the mandibular incisors revealed that the enamel surface of the Smad3 (-/-) mice was irregular and disrupted in places and showed images similar to decalcified mature enamel. The histological analysis of the decalcified sections showed that distinct morphological changes in the ameloblasts at the secretory and maturational stages were not observed between the Smad3 (-/-) and Smad3 (+/-) or wild-type mice, while the enamel matrix was observed in the decalcified sections of the mandibular molars in the Smad3 (-/-) mice. These results suggested that Smad3 was required for enamel biomineralization, and TGF-beta and activin signaling might be critical for its process.
Smad3是一种细胞内信号分子，可介导来自转化生长因子-β（TGF-β）和激活素受体的信号。在本研究中，我们发现了Smad3基因靶向缺失的小鼠中存在牙釉质矿化不足的情况。Smad3（-/-）小鼠的切牙釉质呈白垩色，而野生型或Smad3（+/-）小鼠的釉质为黄棕色。对未脱钙切片的组织学分析表明，Smad3（-/-）小鼠上颌切牙的釉质厚度与野生型和Smad3（+/-）小鼠相似，而Smad3（-/-）小鼠上颌磨牙的釉质在某些部位受到破坏。显微计算机断层扫描（microCT）分析显示，与野生型和Smad3（+/-）小鼠相比，Smad3（-/-）小鼠上颌切牙和下颌磨牙的矿化程度显著降低。对下颌切牙的扫描电子显微镜（SEM）分析显示，Smad3（-/-）小鼠的釉质表面不规则，在某些部位受到破坏，呈现出类似于脱钙成熟釉质的图像。对脱钙切片的组织学分析表明，在Smad3（-/-）与Smad3（+/-）或野生型小鼠之间，未观察到分泌期和成熟期成釉细胞有明显的形态变化，而在Smad3（-/-）小鼠下颌磨牙的脱钙切片中观察到了釉质基质。这些结果表明，Smad3是牙釉质生物矿化所必需的，TGF-β和激活素信号可能对其过程至关重要。
