The cell adhesion molecule nectin-1 is critical for normal enamel formation in mice
The cell adhesion molecule nectin-1 is critical for normal enamel formation in mice
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DOI：
10.1093/hmg/ddn243
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发表时间：
2008-11-15
影响因子：
3.5
通讯作者：
Dixon, Michael J.
中科院分区：
文献类型：
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作者：
Barron, Martin J.;Brookes, Steven J.;Dixon, Michael J.
Nectin-1是免疫球蛋白样粘附分子的亚家族的成员，也是粘附连接的成分。在当前的研究中，我们已经表明缺乏nectin-1的小鼠在门牙牙齿中表现出缺陷的搪瓷形成。尽管nectin-1-null小鼠的切牙是低矿物质的，但牙釉质基质的蛋白质组成却没有改变。虽然在成熟阶段的成年细胞与层中间层的基础细胞（Si）之间的界面上观察到了对Nectin-1的强免疫染色，但在nectin-1-Null小鼠中的不存在与该界面上细胞层的分离相关。在野生型小鼠中，该界面上存在许多大的脱染色体。但是，在突变小鼠中粘附持续存在的地方，脱骨小体较小，较少。蜜蜂已被证明可以调节紧密结的形成。但是，这是第一份报告，表明他们也可能参与对脱糖体组装的法规。重要的是，我们的结果表明，Si-Ameloblast界面的完整性对于正常的搪瓷矿化至关重要。
Nectin-1 is a member of a sub-family of immunoglobulin-like adhesion molecules and a component of adherens junctions. In the current study, we have shown that mice lacking nectin-1 exhibit defective enamel formation in their incisor teeth. Although the incisors of nectin-1-null mice were hypomineralized, the protein composition of the enamel matrix was unaltered. While strong immunostaining for nectin-1 was observed at the interface between the maturation-stage ameloblasts and the underlying cells of the stratum intermedium (SI), its absence in nectin-1-null mice correlated with separation of the cell layers at this interface. Numerous, large desmosomes were present at this interface in wild-type mice; however, where adhesion persisted in the mutant mice, the desmosomes were smaller and less numerous. Nectins have been shown to regulate tight junction formation; however, this is the first report showing that they may also participate in the regulation of desmosome assembly. Importantly, our results show that integrity of the SI-ameloblast interface is essential for normal enamel mineralization.