Supplementary Material for: The Role of Epithelial <b><i>Stat3</i></b> in Amelogenesis during Mouse Incisor Renewal

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 <i>Stat3</i> is expressed in the epithelial component of developing and adult mouse teeth, we generated and analyzed <i>Krt14</i>^Cre/+;<i>Stat3</i>^fl/fl mutant mice in which <i>Stat3</i> 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 analysis and was supported by an increase in the pre-expression distance of enamel-enriched proteins such as amelogenin, ameloblastin, and kallikrein-4. Lastly, scanning electron microscopy 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 <i>Stat3</i> in mice leads to delayed incisor amelogenesis.本研究旨在评估上皮信号转导与转录激活因子3（STAT3）在小鼠切牙成釉过程中的作用。鉴于Stat3基因在发育中和成年小鼠牙齿的上皮组分中表达，我们构建并分析了Krt14^Cre/+;Stat3^fl/fl突变小鼠，该品系小鼠的上皮细胞（包括成釉细胞前体细胞及负责釉质形成的成釉细胞）中Stat3基因被特异性失活。组织学分析显示，与对照组相比，突变体小鼠切牙中的釉质基质含量极少。通过显微计算机断层扫描（micro-computed X-ray tomography）分析证实，突变小鼠切牙釉质矿化存在延迟，且釉原蛋白、成釉蛋白及激肽释放酶-4等釉质富集蛋白的前表达距离延长，进一步支持了该结论。最后，扫描电子显微镜分析显示，第一磨牙近中根下方的突变体小鼠切牙釉质矿化程度极低；但对照组与突变体小鼠切牙的萌出部分，其釉质矿化的微观结构并无显著差异。综上，本研究首次证实，小鼠上皮细胞中Stat3基因的缺失会导致切牙成釉过程延迟。

搜集汇总

背景与挑战

背景概述

该数据集是2018年发布的关于小鼠切牙釉质形成研究的补充材料，主要探讨上皮Stat3基因在釉质生成中的作用。通过分析突变小鼠模型，研究发现Stat3失活会导致釉质矿化延迟和基质减少，但釉质微结构保持相似。数据集属于医学领域，聚焦于牙釉质、转录因子等关键词，为相关生物学研究提供支持。