Special AT‐rich sequence‐binding protein 2 (Satb2) synergizes with Bmp9 and is essential for osteo/odontogenic differentiation of mouse incisor mesenchymal stem cells,Cell Proliferation

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Special AT‐rich sequence‐binding protein 2 (Satb2) synergizes with Bmp9 and is essential for osteo/odontogenic differentiation of mouse incisor mesenchymal stem cells
Cell Proliferation ( IF 5.9 ) Pub Date : 2021-03-04 , DOI: 10.1111/cpr.13016
Qiuman Chen _{1,

2} , Liwen Zheng _{1,

2} , Yuxin Zhang _{1,

2} , Xia Huang _{1,

3} , Feilong Wang _{1,

2} , Shuang Li _{1,

2} , Zhuohui Yang _{1,

2} , Fang Liang _{1,

2} , Jing Hu _{1,

2} , Yucan Jiang _{1,

2} , Yeming Li _{1,

2} , Pengfei Zhou _{1,

3} , Wenping Luo _{1,

3} , Hongmei Zhang _{1,

2}

Affiliation

Mouse incisor mesenchymal stem cells (MSCs) have self‐renewal ability and osteo/odontogenic differentiation potential. However, the mechanism controlling the continuous self‐renewal and osteo/odontogenic differentiation of mouse incisor MSCs remains unclear. Special AT‐rich sequence‐binding protein 2 (SATB2) positively regulates craniofacial patterning, bone development and regeneration, whereas SATB2 deletion or mutation leads to craniomaxillofacial dysplasia and delayed tooth and root development, similar to bone morphogenetic protein (BMP) loss‐of‐function phenotypes. However, the detailed mechanism underlying the SATB2 role in odontogenic MSCs is poorly understood. The aim of this study was to investigate whether SATB2 can regulate self‐renewal and osteo/odontogenic differentiation of odontogenic MSCs.

中文翻译：

特殊的富含 AT 的序列结合蛋白 2 (Satb2) 与 Bmp9 协同作用，对于小鼠门牙间充质干细胞的骨/牙源性分化至关重要

小鼠门牙间充质干细胞（MSC）具有自我更新能力和成骨/牙源性分化潜力。然而，控制小鼠门牙间充质干细胞持续自我更新和成骨/牙源性分化的机制仍不清楚。特殊的富含 AT 的序列结合蛋白 2 (SATB2) 正向调节颅面模式、骨发育和再生，而 SATB2 缺失或突变会导致颅颌面发育不良以及牙齿和牙根发育延迟，类似于骨形态发生蛋白 (BMP) 缺失。功能表型。然而，SATB2 在牙源性 MSC 中作用的详细机制尚不清楚。本研究的目的是探讨 SATB2 是否可以调节牙源性 MSC 的自我更新和骨/牙源性分化。

更新日期：2021-04-02

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