Stem cells of the suture mesenchyme in craniofacial bone development, repair and regeneration.
Stem cells of the suture mesenchyme in craniofacial bone development, repair and regeneration.
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DOI：
10.1038/ncomms10526
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发表时间：
2016-02-01
影响因子：
16.6
通讯作者：
Hsu W
中科院分区：
文献类型：
--
作者：
Maruyama T;Jeong J;Sheu TJ;Hsu W
缝间充质作为颅骨形态发生的生长中心，被假定为骨骼干细胞的微环境。基因调控异常导致缝发育异常，进而引起颅缝早闭，这是最常见的颅面畸形之一。由于各种限制，特别是缺乏缝干细胞的分离方法，大面积颅面骨缺损的修复仍然极具挑战性。在此，我们首次提供证据表明，在颅骨发育和内稳态维持过程中，存在一种表达Axin2的干细胞群，具有长期自我更新、克隆扩增和分化能力。这些细胞位于缝中线，以细胞自主的方式直接参与损伤修复和骨骼再生。我们的研究结果证明它们作为骨骼干细胞的真实身份，具有在细胞治疗中替代受损骨骼的固有能力，并允许进一步阐明干细胞介导的颅面骨骼发生，从而揭示先天性疾病和再生医学的复杂性质。
缝间充质被假定为颅骨干细胞的微环境，但干细胞的身份未知。在此，丸山等人提出，表达Axin2的细胞不仅在颅面骨发育和内稳态中，而且在损伤诱导的修复中充当干细胞。
The suture mesenchyme serves as a growth centre for calvarial morphogenesis and has been postulated to act as the niche for skeletal stem cells. Aberrant gene regulation causes suture dysmorphogenesis resulting in craniosynostosis, one of the most common craniofacial deformities. Owing to various limitations, especially the lack of suture stem cell isolation, reconstruction of large craniofacial bone defects remains highly challenging. Here we provide the first evidence for an Axin2-expressing stem cell population with long-term self-renewing, clonal expanding and differentiating abilities during calvarial development and homeostastic maintenance. These cells, which reside in the suture midline, contribute directly to injury repair and skeletal regeneration in a cell autonomous fashion. Our findings demonstrate their true identity as skeletal stem cells with innate capacities to replace the damaged skeleton in cell-based therapy, and permit further elucidation of the stem cell-mediated craniofacial skeletogenesis, leading to revealing the complex nature of congenital disease and regenerative medicine. The suture mesenchyme has been postulated to act as the niche for stem cells for calvarial bones but the identity of the stem cells is unknown. Here, Maruyama et al. suggest that Axin2 expressing cells act as stem cells not only in craniofacial bone development and homeostasis but in injury-induced repair.