Kallikrein-related peptidase-4 (KLK4): role in enamel formation and revelations from ablated mice.
Kallikrein-related peptidase-4 (KLK4): role in enamel formation and revelations from ablated mice.
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与Kallikrein相关的肽酶4（KLK4）：在消融小鼠的搪瓷形成和启示中的作用。
DOI：
10.3389/fphys.2014.00240
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发表时间：
2014
影响因子：
4
通讯作者：
Simmer JP
中科院分区：
文献类型：
--
作者：
Bartlett JD;Simmer JP
牙釉质的发育是分阶段进行的。在分泌阶段，产生富含蛋白质的软釉质层，其膨胀以达到其最终厚度。在成熟阶段，蛋白质被去除，釉质成熟为体内最坚硬的物质。KLK 4在从分泌到成熟阶段的过渡期间表达，并且其表达在整个成熟过程中持续。KLK 4是一种糖基化的胰凝乳蛋白酶样丝氨酸蛋白酶，其在釉质基质蛋白从硬化的釉质层中排出之前切割釉质基质蛋白。KLK 4突变可导致人类和小鼠的常染色体隐性遗传、非综合征性釉质畸形。Klk4消融的小鼠最初具有正常外观的牙齿，具有全厚度的釉质。然而，牙釉质是柔软的，富含蛋白质。Klk4消融小鼠有三个值得注意的发现：首先，釉质棒从棒间釉质脱落，留下空洞，其中釉质在下面的牙本质表面附近断裂。第二，通常融合形成固体釉质棒的约10，000个微晶在消融的小鼠中不能生长在一起，并且可以从棒中脱落。第三，也是最引人注目的，在消融小鼠中，微晶在宽度和厚度（a轴和b轴）上显著生长，直到它们几乎互锁。微晶生长在明确的釉棒，但互锁被阻止，大概是因为太多的蛋白质残留。传统观点认为，釉质蛋白特异性地结合到釉质晶体的侧面以抑制宽度和厚度的生长，使得薄的带状釉质微晶主要在长度上生长。Klk4消融小鼠的结果表明，该惯例需要更新。提出了一种替代机制，即釉质蛋白质形成一个模具或支持结构，形状和方向的矿物带，因为它们的长度增长。这种支撑结构的残余物必须通过KLK 4去除，以便微晶可以互锁以形成完全硬化的搪瓷。
Enamel development occurs in stages. During the secretory stage, a soft protein rich enamel layer is produced that expands to reach its final thickness. During the maturation stage, proteins are removed and the enamel matures into the hardest substance in the body. KLK4 is expressed during the transition from secretory to the maturation stage and its expression continues throughout maturation. KLK4 is a glycosylated chymotrypsin-like serine protease that cleaves enamel matrix proteins prior to their export out of the hardening enamel layer. Mutations in KLK4 can cause autosomal recessive, non-syndromic enamel malformations in humans and mice. Klk4 ablated mice initially have normal-looking teeth with enamel of full thickness. However, the enamel is soft and protein-rich. Three findings are notable from Klk4 ablated mice: first, enamel rods fall from the interrod enamel leaving behind empty holes where the enamel fractures near the underlying dentin surface. Second, the ~10,000 crystallites that normally fuse to form a solid enamel rod fail to grow together in the ablated mice and can fall out of the rods. Third, and most striking, the crystallites grow substantially in width and thickness (a- and b-axis) in the ablated mice until they almost interlock. The crystallites grow in defined enamel rods, but interlocking is prevented presumably because too much protein remains. Conventional thought holds that enamel proteins bind specifically to the sides of enamel crystals to inhibit growth in width and thickness so that the thin, ribbon-like enamel crystallites grow predominantly in length. Results from Klk4 ablated mice demonstrate that this convention requires updating. An alternative mechanism is proposed whereby enamel proteins serve to form a mold or support structure that shapes and orients the mineral ribbons as they grow in length. The remnants of this support structure must be removed by KLK4 so that the crystallites can interlock to form fully hardened enamel.
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DOI：
10.1155/2013/684607
发表时间：
2013-09-16
期刊：
ISRN dentistry
影响因子：
--
作者：
Bartlett JD
通讯作者：
Bartlett JD
影响因子：
1.9
作者：
Hu Y;Hu JC;Smith CE;Bartlett JD;Simmer JP
通讯作者：
Simmer JP
影响因子：
3
作者：
Beniash, Elia;Metzler, Rebecca A.;Lam, Raymond S. K.;Gilbert, P. U. P. A.
通讯作者：
Gilbert, P. U. P. A.
影响因子：
2.7
作者：
Hu, Jan C. -C.;Chun, Yong-Hee P.;Simmer, James P.
通讯作者：
Simmer, James P.
影响因子：
4.2
作者：
CUISINIER, FJG;STEUER, P;FRANK, RM
通讯作者：
FRANK, RM