The Role of Epithelial Stat3 in Amelogenesis during Mouse Incisor Renewal.

The Role of Epithelial Stat3 in Amelogenesis during Mouse Incisor Renewal.
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DOI:
10.1159/000486745
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发表时间:
2018
期刊:
Cells, tissues, organs
影响因子:
--
通讯作者:
Jheon AH
Jheon AH
中科院分区:
其他
文献类型:
--
作者:
Zhang B;Meng B;Viloria E;Naveau A;Ganss B;Jheon AH

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本研究旨在探讨上皮细胞信号转导子和转录激活子3(STAT 3)在小鼠切牙成釉过程中的作用。由于Stat 3在发育和成年小鼠牙齿的上皮成分中表达,我们产生并分析了Krt 14 Cre/+; Stat 3fl/fl突变小鼠,其中Stat 3在上皮细胞中失活,包括成釉细胞祖细胞和成釉细胞-负责釉质形成的细胞。组织学分析显示,与对照组相比,突变体切牙的釉质基质很少。使用微型计算机X射线断层扫描(microCT)分析证明了延迟的切牙釉质矿化,并通过增加釉质富集蛋白(如釉原蛋白(AMEL),成釉蛋白(AMBN)和激肽释放酶4(KLK 4))的表达距离来支持。最后,扫描电子显微镜(SEM)分析显示,在第一磨牙的近中根下的突变体切牙中几乎没有釉质矿化,然而,釉质矿化的微结构在对照和突变体切牙的萌出部分是相似的。综上所述,我们的研究结果首次证明,上皮细胞Stat 3的缺乏导致小鼠切牙釉质形成延迟。
The aim of this study was to evaluate the role of epithelial Signal transducer and activator of transcription 3 (STAT3) in mouse incisor amelogenesis. Since Stat3 is expressed in the epithelial component of developing and adult mouse teeth, we generated and analyzed Krt14Cre/+;Stat3fl/fl mutant mice in which Stat3 was inactivated in epithelia including ameloblast progenitors and ameloblasts – the cells responsible for enamel formation. Histological analysis showed little enamel matrix in mutant incisors compared to controls. Delayed incisor enamel mineralization was demonstrated using micro-computed X-ray tomography (microCT) analysis and was supported by an increase in the pre-expression distance of enamel-enriched proteins such as amelogenin (AMEL), ameloblastin (AMBN), and Kallikrein4 (KLK4). Lastly, scanning electron microscopy (SEM) analysis showed little enamel mineralization in mutant incisors underneath the mesial root of the 1st molar, however, the micro-architecture of enamel mineralization was similar in the erupted portion of control and mutant incisors. Taken together, our findings demonstrate for the first time that the absence of epithelial Stat3 in mice leads to delayed incisor amelogenesis.
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