Why Does Enamel in Klk4-Null Mice Break above the Dentino-Enamel Junction?

Why Does Enamel in Klk4-Null Mice Break above the Dentino-Enamel Junction?
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DOI:
10.1159/000324260
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发表时间:
2011-01-01
影响因子:
2.7
通讯作者:
Hu, Jan C. -C.
Hu, Jan C. -C.
中科院分区:
生物学4区
文献类型:
--
作者:
Simmer, James P.;Hu, Yuanyuan;Hu, Jan C. -C.

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背景:激肽释放酶4(KLK4)基因缺失小鼠的釉质层厚度正常,釉质棒状交叉排列,但含有残留的釉质蛋白,矿化程度较低,最深处就在牙本质-牙釉质连接处(DEJ)上方断裂。断裂平面令人费解,因为最深的釉质是最早沉积的,并且在分泌期釉质蛋白酶(MMP20)的作用下,是Klk4表达开始时釉质层最成熟的部分。目的:研究MMP20和Klk4基因缺失小鼠的骨折平面,并对Klk4在发育中牙齿中的表达进行定位。方法:7周龄时处死Klk4基因缺失和MMP20基因缺失的小鼠,用扫描电子显微镜观察其下颌切牙形态结构。Klk4(+/LacZ)小鼠与Klk4(+/LacZ)小鼠交配。用聚合酶链式反应对后代进行基因分型。对出生后第5、8、11和14天的KLK(4+/+)、KLK4(+/LacZ)和KLK4(LacZ/LacZ)(空)产仔进行β-半乳糖苷酶组织化学分析。结果:MMP20基因缺失小鼠的釉质层在DEJ处断裂,Klk4基因缺失小鼠的釉质层断裂发生在DEJ以上。KLK4在分泌期的成釉细胞、分泌期以下的小鼠成牙本质细胞和成熟期的成釉细胞中不表达。KLK4在过渡期和成熟期成釉细胞中特异表达。结论:Klk4基因缺失小鼠DEJ附近的釉质断裂不是由于成牙本质细胞表达Klk4的失败所致,而是与釉质深度进行性低矿化有关。版权所有(C)2011 S.Karger AG,巴塞尔
Background: The enamel layer of kallikrein 4 (Klk4)-null mice has a normal thickness and a decussating pattern of enamel rods, but it contains residual enamel proteins, is less highly mineralized, and fractures in its deepest part just above the dentino-enamel junction (DEJ). The plane of fracture is puzzling because the deepest enamel is deposited earliest and, through the action of the secretory stage enamel protease (Mmp20), is the most mature part of the enamel layer at the time of the onset of Klk4 expression. Objectives: To characterize the planes of fracture in Mmp20- and Klk4 -null mice and to localize Klk4 expression in developing teeth. Methods: Klk4- and Mmp20 -null mice were sacrificed at 7 weeks and their mandibular incisors were characterized by scanning electron microscopy. Klk4(+/lacZ) mice were mated with Klk4(+/lacZ) mice. Offspring were genotyped by polymerase chain reaction. Klk(4+/+), Klk4(+/lacZ), and Klk4(lacZ/lacZ) (null) littermates on postnatal days 5, 8, 11, and 14 were processed for beta-galactosidase histochemistry. Results: The enamel layer fractures at the DEJ in Mmp20 -null mice, and fractures occur in enamel above the DEJ in Klk4 -null mice. Klk4 is not expressed by secretory-stage ameloblasts, murine odontoblasts beneath the secretory stage, or maturation-stage ameloblasts. Klk4 is specifically expressed by transition and maturation-stage ameloblasts. Conclusions: The breakage of enamel near the DEJ in Klk4-null mice is not due to a failure of odontoblasts to express Klk4, but it relates to a progressive hypomineralization of enamel with depth. Copyright (C) 2011 S. Karger AG, Basel