Bcl11b transcription factor plays a role in the maintenance of the ameloblast-progenitors in mouse adult maxillary incisors
Bcl11b transcription factor plays a role in the maintenance of the ameloblast-progenitors in mouse adult maxillary incisors
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DOI：
10.1016/j.mod.2013.05.002
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发表时间：
2013-09-01
影响因子：
2.6
通讯作者：
Kominami, Ryo
中科院分区：
文献类型：
--
作者：
Katsuragi, Yoshinori;Anraku, Junko;Kominami, Ryo
啮齿动物的门牙保持着持续生长的能力，它们的唇侧牙本质被釉质覆盖。Bcl 11b锌指转录因子在小鼠切牙的成釉细胞祖细胞中表达，其在Bcl 11b（KO/KO）小鼠中的缺失导致胚胎牙齿发育缺陷。然而，由于Bcl 11b（KO/KO）小鼠出生时死亡，因此未研究Bcl 11b在成年组织中切牙维持中的作用。在这里，我们研究了复合杂合子Bcl 11b（S826 G/KO）小鼠，其中一个等位基因具有氨基酸取代丝氨酸在位置826甘氨酸，表现出发育不全的上颌切牙与较低浓度的矿物质在釉质和牙本质，伴随着上颌骨发育不全。组织学检查发现切牙唇颈环发育不全，成釉细胞祖细胞区缩短，成釉细胞系细胞分化和增殖受损。然而，有趣的是，出生后5天的幼年小鼠在这些表型上没有显示出明显的变化。这些结果表明，衰减Bcl 11b活性损害成釉细胞祖细胞和门牙的维护。Bcl 11b（S826 G/KO）切牙中BrdU标记保留细胞（假定的干细胞）的数量较低，这表明切牙发育不全可能部分是干细胞数量减少的结果。有趣的是，Shh和FGF 3的表达水平，这被认为是在成釉细胞和成牙本质细胞的发育和维护中发挥关键作用，并没有减少，虽然表达区域更局限于成釉细胞祖细胞和间充质区域的Bcl 11b（S826 G/KO）切牙，分别。这些数据表明，Bcl 11b的门牙维护是不直接相关的FGF上皮间充质信号循环，包括Shh，但内在的成釉细胞祖细胞和可能的干细胞。(C)2013爱思唯尔爱尔兰有限公司版权所有。
Rodent incisors maintain the ability to grow continuously and their labial dentin is covered with enamel. Bcl11b zinc-finger transcription factor is expressed in ameloblast progenitors in mouse incisors and its absence in Bcl11b(KO/KO) mice results in a defect in embryonic tooth development. However, the role of Bcl11b in incisor maintenance in adult tissue was not studied because of death at birth in Bcl11b(KO/KO) mice. Here, we examined compound heterozygous Bcl11b(S826G/KO) mice, one allele of which has an amino acid substitution of serine at position 826 for glycine, that exhibited hypoplastic maxillary incisors with lower concentrations of minerals at the enamel and the dentin, accompanying the maxillary bone hypoplasia. Histological examinations revealed hypoplasia of the labial cervical loop in incisors, shortening of the ameloblast progenitor region, and impairment in differentiation and proliferation of ameloblast-lineage cells. Interestingly, however, juvenile mice at 5 days after birth did not show marked change in these phenotypes. These results suggest that attenuated Bcl11b activity impairs ameloblast progenitors and incisor maintenance. The number of BrdU label-retaining cells, putative stem cells, was lower in Bcl11b(S826G/KO) incisors, which suggests the incisor hypoplasia may be in part a result of the decreased number of stem cells. Interestingly, the level of Shh and FGF3 expressions, which are assumed to play key roles in the development and maintenance of ameloblasts and odontoblasts, was not decreased, though the expressed areas were more restricted in ameloblast progenitor and mesenchyme regions of Bcl11b(S826G/KO) incisors, respectively. Those data suggest that the incisor maintenance by Bcl11b is not directly related to the FGF epithelial-mesenchymal signaling loop including Shh but is intrinsic to ameloblast progenitors and possibly stem cells. (C) 2013 Elsevier Ireland Ltd. All rights reserved.