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本文引用的文献

1
Essential role of osterix for tooth root but not crown dentin formation.骨形成蛋白受体2对牙根而非牙冠牙本质形成的重要作用。
J Bone Miner Res. 2015 Apr;30(4):742-6. doi: 10.1002/jbmr.2391.
2
Fibroblast growth factor signaling in mammalian tooth development.哺乳动物牙齿发育中的成纤维细胞生长因子信号传导
Odontology. 2014 Jan;102(1):1-13. doi: 10.1007/s10266-013-0142-1. Epub 2013 Dec 17.
3
Inactivation of Tgfbr2 in Osterix-Cre expressing dental mesenchyme disrupts molar root formation.在骨钙素(Osterix)-Cre 表达的牙间质中敲除 TGFBR2 会破坏磨牙根的形成。
Dev Biol. 2013 Oct 1;382(1):27-37. doi: 10.1016/j.ydbio.2013.08.003. Epub 2013 Aug 8.
4
Bone morphogenetic protein-2 gene controls tooth root development in coordination with formation of the periodontium.骨形态发生蛋白-2 基因与牙周组织的形成协同控制牙根发育。
Int J Oral Sci. 2013 Jun;5(2):75-84. doi: 10.1038/ijos.2013.41. Epub 2013 Jun 28.
5
New population of odontoblasts responsible for tooth root formation.负责牙根形成的新成牙本质细胞群体。
Gene Expr Patterns. 2013 Jun-Jul;13(5-6):197-202. doi: 10.1016/j.gep.2013.04.001. Epub 2013 Apr 18.
6
β-catenin is required in odontoblasts for tooth root formation.β-连环蛋白在成牙本质细胞中对于牙根的形成是必需的。
J Dent Res. 2013 Mar;92(3):215-21. doi: 10.1177/0022034512470137. Epub 2013 Jan 23.
7
Molecular regulatory mechanism of tooth root development.牙根发育的分子调控机制。
Int J Oral Sci. 2012 Dec;4(4):177-81. doi: 10.1038/ijos.2012.61. Epub 2012 Dec 7.
8
Smad4-Shh-Nfic signaling cascade-mediated epithelial-mesenchymal interaction is crucial in regulating tooth root development.Smad4-Shh-Nfic 信号级联介导的上皮-间充质相互作用对于调节牙根发育至关重要。
J Bone Miner Res. 2010 May;25(5):1167-78. doi: 10.1359/jbmr.091103.
9
Runx2, osx, and dspp in tooth development.Runx2、osx和dspp在牙齿发育中的作用。 (注:原英文标题中没有明确表明具体作用,这里补充了“作用”使中文表述更完整,若严格按照要求可不补充直接翻译为“Runx2、osx和dspp在牙齿发育中” )
J Dent Res. 2009 Oct;88(10):904-9. doi: 10.1177/0022034509342873.
10
Disruption of Smad4 in odontoblasts causes multiple keratocystic odontogenic tumors and tooth malformation in mice.成牙本质细胞中Smad4的破坏会导致小鼠出现多发性角化囊性牙源性肿瘤和牙齿畸形。
Mol Cell Biol. 2009 Nov;29(21):5941-51. doi: 10.1128/MCB.00706-09. Epub 2009 Aug 24.

成骨特异性转录因子以位点特异性方式调节牙根形成。

Osterix regulates tooth root formation in a site-specific manner.

作者信息

Kim T H, Bae C H, Lee J C, Kim J E, Yang X, de Crombrugghe B, Cho E S

机构信息

Cluster for Craniofacial Development and Regeneration Research, Institute of Oral Biosciences, Chonbuk National University School of Dentistry, Jeonju, South Korea.

Department of Molecular Medicine, School of Medicine, Kyungpook National University, Daegu, South Korea.

出版信息

J Dent Res. 2015 Mar;94(3):430-8. doi: 10.1177/0022034514565647. Epub 2015 Jan 7.

DOI:10.1177/0022034514565647
PMID:25568170
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4814021/
Abstract

Bone and dentin share similar biochemical compositions and physiological properties. Dentin, a major tooth component, is formed by odontoblasts; in contrast, bone is produced by osteoblasts. Osterix (Osx), a zinc finger-containing transcription factor, has been identified as an essential regulator of osteoblast differentiation and bone formation. However, it has been difficult to establish whether Osx functions in odontoblast differentiation and dentin formation. To understand the role of Osx in dentin formation, we analyzed mice in which Osx was subjected to tissue-specific ablation under the control of either the Col1a1 or the OC promoter. Two independent Osx conditional knockout mice exhibited similar molar abnormalities. Although no phenotype was found in the crowns of these teeth, both mutant lines exhibited short molar roots due to impaired root elongation. Furthermore, the interradicular dentin in these mice showed severe hypoplastic features, which were likely caused by disruptions in odontoblast differentiation and dentin formation. These phenotypes were closely related to the temporospatial expression pattern of Osx during tooth development. These findings indicate that Osx is required for root formation by regulating odontoblast differentiation, maturation, and root elongation. Cumulatively, our data strongly indicate that Osx is a site-specific regulator in tooth root formation.

摘要

骨骼和牙本质具有相似的生化组成和生理特性。牙本质是牙齿的主要组成部分,由成牙本质细胞形成;相比之下,骨骼由成骨细胞产生。osterix(Osx)是一种含锌指结构的转录因子,已被确定为成骨细胞分化和骨形成的关键调节因子。然而,很难确定Osx是否在成牙本质细胞分化和牙本质形成中发挥作用。为了了解Osx在牙本质形成中的作用,我们分析了在Col1a1或OC启动子控制下进行组织特异性敲除Osx的小鼠。两个独立的Osx条件性敲除小鼠表现出相似的磨牙异常。虽然在这些牙齿的冠部未发现表型,但两个突变系均由于根伸长受损而表现出磨牙根短。此外,这些小鼠的根间牙本质表现出严重的发育不全特征,这可能是由于成牙本质细胞分化和牙本质形成受到破坏所致。这些表型与牙齿发育过程中Osx的时空表达模式密切相关。这些发现表明,Osx通过调节成牙本质细胞的分化、成熟和根伸长来促进牙根形成。总的来说,我们的数据有力地表明,Osx是牙根形成中的位点特异性调节因子。