Colonization of the Satellite Cell Niche by Skeletal Muscle Progenitor Cells Depends on Notch Signals
Colonization of the Satellite Cell Niche by Skeletal Muscle Progenitor Cells Depends on Notch Signals
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DOI：
10.1016/j.devcel.2012.07.014
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发表时间：
2012-09-11
影响因子：
11.8
通讯作者：
Birchmeier, Carmen
中科院分区：
文献类型：
--
作者：
Broehl, Dominique;Vasyutina, Elena;Birchmeier, Carmen
骨骼肌的生长和再生依赖于生肌祖细胞和卫星细胞，即出生后肌肉的干细胞。在小鼠发育过程中，Notch信号的消除会导致肌源性祖细胞的过早分化和非常小的肌群的形成。在这里，我们表明这种剧烈的影响是由肌肉分化因子MyoD的突变拯救的。然而，获救的肌原性祖细胞不具有卫星细胞的位置，对肌纤维生长的贡献不大。归巢的中断是由于新生卫星细胞周围的基底层组装缺陷以及它们与肌纤维的粘附受损。在分子水平上，新生卫星细胞解除了对基底层成分和粘附分子（如整合素α 7、胶原XVIII α 1、Megf10和Mcam）表达的调控。我们得出结论，Notch信号控制卫星细胞的归巢，刺激它们为自己的微环境做出贡献并粘附在肌纤维上。
Skeletal muscle growth and regeneration rely on myogenic progenitor and satellite cells, the stem cells of postnatal muscle. Elimination of Notch signals during mouse development results in premature differentiation of myogenic progenitors and formation of very small muscle groups. Here we show that this drastic effect is rescued by mutation of the muscle differentiation factor MyoD. However, rescued myogenic progenitors do not assume a satellite cell position and contribute poorly to myofiber growth. The disrupted homing is due to a deficit in basal lamina assembly around emerging satellite cells and to their impaired adhesion to myofibers. On a molecular level, emerging satellite cells deregulate the expression of basal lamina components and adhesion molecules like integrin alpha 7, collagen XVIII alpha 1, Megf10, and Mcam. We conclude that Notch signals control homing of satellite cells, stimulating them to contribute to their own microenvironment and to adhere to myofibers.