A new role for satellite cells: control of reinnervation after muscle injury by semaphorin 3A. Focus on "Possible implication of satellite cells in regenerative motoneuritogenesis: HGF upregulates neural chemorepellent Sema3A during myogenic differentiati
A new role for satellite cells: control of reinnervation after muscle injury by semaphorin 3A. Focus on "Possible implication of satellite cells in regenerative motoneuritogenesis: HGF upregulates neural chemorepellent Sema3A during myogenic differentiati
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卫星细胞的新作用：信号蛋白 3A 控制肌肉损伤后的神经支配。
DOI：
10.1152/ajpcell.00256.2009
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发表时间：
2009
期刊：
影响因子：
--
通讯作者：
McLoon,LindaK
中科院分区：
文献类型：
--
作者：
McLoon,LindaK
IN THE ALMOST 50 YEARS SINCE Mauro (21) first identified satellite cells in mature skeletal muscle, a great deal has been discovered about the role these myogenic precursor cells play in muscle repair and regeneration. Skeletal muscle regeneration involves coordination of a number of processes in the injured muscles. Not only do injured and/or dying myofibers need to be repaired and/or replaced, but these regenerating myofibers need to be appropriately innervated and vascularized. In muscle disease and after certain forms of denervation injury, muscle regenerative capacity is impaired. Understanding the control of the regenerative population in adult skeletal muscle, the satellite cells, will allow the development of successful strategies to improve return of function after injury or in disease.A great many experiments have focused on understanding what controls satellite cell function in adult muscle during regeneration after injury. The first step is the activation of these normally quiescent satellite cells so that they enter the cell cycle. In an extremely novel series of studies, Anderson, Tatsumi, and Allen identified two of the earliest signaling molecules involved in activating these cells to divide. First, nitric oxide (NO) is released locally at the point of injury, serving as the initial activator of satellite cells to enter the cell cycle (5). Following NO activation of the satellite cells, hepatocyte growth factor (HGF) is released from damaged myofibers, binds to c-met receptors on the satellite cells, and stimulates those that are distant from the initial site of injury to proliferate (4). The satellite cells themselves begin to secrete HGF, thus maintaining their activated state through an autocrine feedback loop. HGF also stimulates satellite cell migration toward the site of the injured muscle, another critical factor in enhancing muscle regeneration after injury (7). Ultimately, new myofibers are formed by fusion of satellite cells to form myotubes; additionally, the activated satellite cells can repair damaged myofibers by fusing directly with them. These events were confirmed using irradiation, which abrogates the regenerative response (16), and tritiated thymidine labeling, demonstrating fusion of muscle precursors to form new myofibers (22).
