The molecular responses of skeletal muscle satellite cells to continuous expression of IGF-1: Implications for the rescue of induced muscular atrophy in aged rats
The molecular responses of skeletal muscle satellite cells to continuous expression of IGF-1: Implications for the rescue of induced muscular atrophy in aged rats
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DOI：
10.1123/ijsnem.11.s1.s44
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发表时间：
2001-12-01
影响因子：
2.5
通讯作者：
Spangenburg, EE
中科院分区：
文献类型：
--
作者：
Chakravarthy, MV;Booth, FW;Spangenburg, EE
大约50%的85岁以上的人由于骨骼肌虚弱而身体虚弱。这表明需要确定解决这一问题的机制。出生后肌肉生长的一个关键细胞因子是一群生肌前体细胞，称为卫星细胞。考虑到肌肉减少症的复杂过程，有人假设，在这个过程中的某个时刻，有限的卫星细胞增殖潜力可能会限制旧肌肉的再生。可以想象，如果卫星细胞增殖能力可以随着年龄的增长而保持或增强，那么肌肉减少症可能会被延迟或预防。因此，本文的目的是描述胰岛素样生长因子-I是否可以防止由后肢固定的重复循环引起的肌肉萎缩，增加这些肌肉的卫星细胞的体外增殖，如果是这样，胰岛素样生长因子-I介导这种增加的增殖的分子机制。我们的研究结果提供了证据表明，IGF-I可能通过增加卫星细胞增殖来促进老年肌肉再生。结果还表明，IGF-I通过PI 3 '-K/Akt途径降低细胞周期抑制因子p27（Kip 1），从而增强卫星细胞增殖。这些数据为IGF-I对衰老相关的骨骼肌萎缩的拯救作用提供了分子证据。
Approximately 50% of humans older than 85 years have physical frailty due to weak skeletal muscles. This indicates a need for determining mechanisms to combat this problem. A critical cellular factor for postnatal muscle growth is a population of myogenic precursor cells called satellite cells. Given the complex process of sarcopenia, it has been postulated that, at some point in this process, a limited satellite cell proliferation potential could become rate-limiting to the regrowth of old muscles. It is conceivable that if satellite cell proliferative capacity can be maintained or enhanced with advanced age, sarcopenia could potentially be delayed or prevented. Therefore, the purposes of this paper are to describe whether IGF-I can prevent muscular atrophy induced by repeated cycles of hindlimb immobilization, increase the in vitro proliferation in satellite cells from these muscles and, if so, the molecular mechanisms by which IGF-I mediates this increased proliferation. Our results provide evidence that IGF-I can enhance aged muscle regrowth possibly through increased satellite cell proliferation. The results also suggest that IGF-I enhances satellite cell proliferation by decreasing the cell cycle inhibitor, p27(Kip1) through the PI3'-K/Akt pathway. These data provide molecular evidence for IGF-I's rescue effect upon aging-associated skeletal muscle atrophy.