The suture provides a niche for mesenchymal stem cells of craniofacial bones.
The suture provides a niche for mesenchymal stem cells of craniofacial bones.
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DOI：
10.1038/ncb3139
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发表时间：
2015-04
影响因子：
21.3
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中科院分区：
文献类型：
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骨组织在干细胞的支持下不断更新。最近的研究表明，血管周围间充质干细胞（MSCs）有助于长骨的更新。颅面骨是源自与长骨不同的胚胎起源的扁平骨。颅面骨间充质干细胞的身份和调控生态位尚不清楚。在这里，我们确定Gli 1+细胞缝间充质内的主要MSC人口颅面骨。它们不与脉管系统相关，在成人中产生所有颅面骨，并在损伤修复期间被激活。Gli 1+细胞是体外典型的MSC。Gli 1+细胞的消融导致颅缝早闭和颅骨生长停滞，表明这些细胞是不可或缺的干细胞群。患有颅缝早闭的Twist 1 +/−小鼠在缝线中显示Gli 1 + MSC减少，表明颅缝早闭可能是由缝线干细胞减少引起的。我们的研究表明，颅面缝提供了一个独特的生态位，骨髓间充质干细胞颅面骨的稳态和修复。
Bone tissue undergoes constant turnover supported by stem cells. Recent studies showed that perivascular mesenchymal stem cells (MSCs) contribute to the turnover of long bones. Craniofacial bones are flat bones derived from a different embryonic origin than the long bones. The identity and regulating niche for craniofacial bone MSCs remain unknown. Here, we identify Gli1+ cells within the suture mesenchyme as the major MSC population for craniofacial bones. They are not associated with vasculature, give rise to all craniofacial bones in the adult and are activated during injury repair. Gli1+ cells are typical MSCs in vitro. Ablation of Gli1+ cells leads to craniosynostosis and arrest of skull growth, indicating these cells are an indispensible stem cell population. Twist1+/− mice with craniosynostosis show reduced Gli1+ MSCs in sutures, suggesting that craniosynostosis may result from diminished suture stem cells. Our study indicates that craniofacial sutures provide a unique niche for MSCs for craniofacial bone homeostasis and repair.