Dental enamel development: proteinases and their enamel matrix substrates.
Dental enamel development: proteinases and their enamel matrix substrates.
复制标题
DOI：
10.1155/2013/684607
复制
发表时间：
2013-09-16
期刊：
影响因子：
--
通讯作者：
Bartlett JD
中科院分区：
文献类型：
--
作者：
Bartlett JD
这篇综述集中在最近的发现和深入详细了解什么是已知的每一种蛋白质（釉原蛋白，成釉蛋白和釉蛋白）和蛋白酶（基质金属蛋白酶-20和激肽释放酶相关的肽酶-4）分泌到釉质基质。在概述了釉质发育之后，本文着重介绍了这些釉质蛋白的命名、组织表达、功能、蛋白酶激活和蛋白酶底物特异性。这些蛋白质和它们各自的无效小鼠和人类的突变也进行了评估，以阐明机制，导致非综合征性釉质畸形称为釉质发生的突变。相关争议得到解决。例如，这些蛋白质中的任何一种除了在釉质发育中的作用外，还具有关键功能吗？釉原蛋白是否启动微晶生长，是否抑制微晶宽度和厚度的生长，还是两者都不起作用？对空小鼠文献的详细检查为这些问题提供了明确的线索和/或答案，并对这些数据进行了彻底的分析。这项分析得出的惊人结论表明，广泛持有的釉质形成的范例是不够的。本文的最后一部分将最近的数据编织成一个合理的新机制，这些釉基质蛋白支持和促进釉质发育。
This review focuses on recent discoveries and delves in detail about what is known about each of the proteins (amelogenin, ameloblastin, and enamelin) and proteinases (matrix metalloproteinase-20 and kallikrein-related peptidase-4) that are secreted into the enamel matrix. After an overview of enamel development, this review focuses on these enamel proteins by describing their nomenclature, tissue expression, functions, proteinase activation, and proteinase substrate specificity. These proteins and their respective null mice and human mutations are also evaluated to shed light on the mechanisms that cause nonsyndromic enamel malformations termed amelogenesis imperfecta. Pertinent controversies are addressed. For example, do any of these proteins have a critical function in addition to their role in enamel development? Does amelogenin initiate crystallite growth, does it inhibit crystallite growth in width and thickness, or does it do neither? Detailed examination of the null mouse literature provides unmistakable clues and/or answers to these questions, and this data is thoroughly analyzed. Striking conclusions from this analysis reveal that widely held paradigms of enamel formation are inadequate. The final section of this review weaves the recent data into a plausible new mechanism by which these enamel matrix proteins support and promote enamel development.