表皮生长因子缺陷小鼠牙本质分化紊乱和牙本质发育不良

Lucia Jiménez-Rojo, Susana de Vega, Gaskon Ibarretxe, Takashi Nakamura, Fernando J Unda
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引用次数: 0

摘要

牙齿的形成过程受到上皮组织和间充质组织之间相互影响的严格调控。这些上皮-间质相互作用通过转录因子调控目标基因的表达。在这一过程的调控因子中,Epiprofin/Sp6 是一种锌指转录因子,在胚胎牙上皮和分化前牙本质中均有表达。Epiprofin 基因敲除(Epfn-/-)小鼠表现出严重的牙齿异常,如超常牙齿和釉质发育不全。在这里,我们描述了 Epfn-/- 小鼠臼齿和门齿的牙本质缺陷。我们观察到,在Epfn缺失的情况下,早期牙本质分化的标志物,如碱性磷酸酶活性、Dsp/Dpp表达和胶原蛋白I型沉积都会下调。此外,在发育中的Epfn-/-臼齿的前颌骨细胞层中,紧密连接蛋白和间隙连接蛋白的表达严重受损。总之,我们的数据表明,Epfn对牙齿间充质细胞向功能性牙本质细胞的适当分化以及随后的牙本质基质沉积至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Disrupted odontoblast differentiation and dentin dysplasia in Epiprofin-deficient mice.

Tooth formation is a process tightly regulated by reciprocal interactions between epithelial and mesenchymal tissues. These epithelial-mesenchyme interactions regulate the expression of target genes via transcription factors. Among the regulatory elements governing this process, Epiprofin/Sp6 is a zinc finger transcription factor which is expressed in the embryonic dental epithelium and in differentiating pre-odontoblasts. Epiprofin knockout (Epfn-/-) mice present severe dental abnormalities, such as supernumerary teeth and enamel hypoplasia. Here, we describe dentin defects in molars and incisors of Epfn-/- mice. We observed that in the absence of Epfn, markers of early odontoblast differentiation, such as alkaline phosphatase activity, Dsp/Dpp expression, and Collagen Type I deposition, are downregulated. In addition, the expression of tight and gap junction proteins was severely impaired in the predontoblastic cell layer of developing Epfn-/- molars. Altogether, our data shows that Epfn is crucial for the proper differentiation of dental mesenchymal cells towards functional odontoblasts and subsequent dentin-matrix deposition.

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