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首页> 外文期刊>Biochemical and Biophysical Research Communications >Disruption of Smad4 in odontoblasts and dental epithelial cells influences the phenotype of multiple keratocystic odontogenic tumors
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Disruption of Smad4 in odontoblasts and dental epithelial cells influences the phenotype of multiple keratocystic odontogenic tumors

机译：成牙本质细胞和牙齿上皮细胞中Smad4的破坏影响多种角化囊性牙源性肿瘤的表型

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Keratocystic odontogenic tumors (KCOTs) are cystic epithelial neoplasms with a high recurrence rate. The molecular mechanisms underlying the initiation and progression of KCOTs are still largely unknown. Previous research showed that specific ablation of Smad4 in odontoblasts and dental epithelia resulted in spontaneous KCOTs in mice, and that constitutively activated Hedgehog (Hh) signaling was detected in the cyst epithelia of both Smad4(Co/Co) OC-Cre and Smad4(Co/Co) K5-Cre mice. Here, we ablated Smad4 in mouse odontoblasts and dental epithelia and compared the sizes and numbers of KCOTs. Both the number and size of KCOTs in Smad4(Co/Co) OC-Cre mice were larger than those in Smad4(Co/Co) K5-Cre mice, suggesting that paracrine signals from root odontoblasts play a more important role than those from Hertwig's epithelial root sheath (HERS) cells. (C) 2015 Elsevier Inc. All rights reserved.
机译：角化囊性牙源性肿瘤（KCOT）是具有高复发率的囊性上皮性肿瘤。 KCOTs发生和发展的分子机制仍是未知之数。先前的研究表明，成牙本质细胞和牙齿上皮细胞中Smad4的特异性消融导致小鼠自发性KCOTs，并且在Smad4（Co / Co）OC-Cre和Smad4（Co）的囊肿上皮中检测到组成型激活的刺猬（Hh）信号传导。 / Co）K5-Cre小鼠。在这里，我们消融了小鼠成牙本质细胞和牙齿上皮细胞中的Smad4，并比较了KCOT的大小和数量。 Smad4（Co / Co）OC-Cre小鼠的KCOT数量和大小均大于Smad4（Co / Co）K5-Cre小鼠，这表明来自成牙本质成牙根细胞的旁分泌信号比来自Hertwig's的旁分泌信号更重要。上皮根鞘（HERS）细胞。 （C）2015 Elsevier Inc.保留所有权利。

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