Cellular and molecular responses to increased skeletal muscle loading after irradiation
Cellular and molecular responses to increased skeletal muscle loading after irradiation
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DOI：
10.1152/ajpcell.00173.2002
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发表时间：
2002-10-01
影响因子：
5.5
通讯作者：
Baldwin, KM
中科院分区：
文献类型：
--
作者：
Adams, GR;Caiozzo, VJ;Baldwin, KM
在增加负荷之前对大鼠骨骼肌进行照射，已被证明可以防止长达4周的代偿性肥大，可能是通过防止卫星细胞增殖和提供新的肌核。最近的研究表明，干细胞群的存在可能会使受辐射的肌肉最终随着时间的推移而肥大。我们报道，照射基本上防止了3mo功能性超负荷(OL-ir)引起的大鼠肌肉肥大。在前3-7天，OL-ir和对侧未受照射的超负荷(OL)肌肉的合成代谢和肌源性反应的细胞和分子标志物的变化的时间进程和幅度相似。然后，这些标记物在OL-IR肌肉中恢复到对照水平，而在OL肌肉中保持升高。OL肌的肌核数目和DNA含量明显增加，而OL-IR肌的DNA含量无明显变化。因此，在这段时间内，干细胞似乎没有被添加到受照射的肌肉中。这些数据与大鼠代偿性肥大可能需要增加新的肌核的理论一致。
Irradiation of rat skeletal muscles before increased loading has been shown to prevent compensatory hypertrophy for periods of up to 4 wk, possibly by preventing satellite cells from proliferating and providing new myonuclei. Recent work suggested that stem cell populations exist that might allow irradiated muscles to eventually hypertrophy over time. We report that irradiation essentially prevented hypertrophy in rat muscles subjected to 3 mo of functional overload (OL-Ir). The time course and magnitude of changes in cellular and molecular markers of anabolic and myogenic responses were similar in the OL-Ir and the contralateral nonirradiated, overloaded (OL) muscles for the first 3-7 days. These markers then returned to control levels in OL-Ir muscles while remaining elevated in OL muscles. The number of myonuclei and amount of DNA were increased markedly in OL but not OL-Ir muscles. Thus it appears that stem cells were not added to the irradiated muscles in this time period. These data are consistent with the theory that the addition of new myonuclei may be required for compensatory hypertrophy in the rat.