Apoptosis: a mechanism contributing to remodeling of skeletal muscle in response to hindlimb unweighting
Apoptosis: a mechanism contributing to remodeling of skeletal muscle in response to hindlimb unweighting
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DOI：
10.1152/ajpcell.1997.273.2.c579
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发表时间：
1997-08-01
影响因子：
5.5
通讯作者：
Edgerton, VR
中科院分区：
文献类型：
--
作者：
Allen, DL;Linderman, JK;Edgerton, VR
研究了细胞凋亡在后肢卸载引起的肌肉萎缩中肌核消除中的作用以及细胞凋亡的抑制在预防肌肉萎缩中的作用。通过末端脱氧核苷酸转移酶（TDT）组织化学染色显示，细胞凋亡指标双链DNA断裂的细胞核数量在悬浮14天后显著增加。TDT和抗层粘连蛋白免疫组化双重染色显示部分TDT阳性核位于纤维层内，很可能是肌核。与对照大鼠相比，悬浮大鼠含有形态异常核的纤维数量也显著增加。生长激素和胰岛素样生长因子I （GH/IGF-I）联合抗阻运动可降低tdt阳性核的增加（相似值为26%，P < 0.05），并显著减少形态异常核的纤维数量。数据表明，1)“程序性核死亡”有助于消除肌核和/或萎缩纤维中的卫星细胞，2)GH/IGF-I给药加肌肉负荷可改善与后肢卸载相关的细胞凋亡。
The role of apoptosis in the elimination of myonuclei during hindlimb unloading-induced atrophy and the inhibition of apoptosis in the prevention of muscle atrophy were examined. The number of nuclei demonstrating double-stranded DNA fragmentation seen by terminal deoxynucleotidyl transferase (TDT) histochemical staining, an indicator of apoptosis, was significantly increased after 14 days of suspension. Double staining with TDT and antilaminin immunohistochemistry revealed that some TDT-positive nuclei were within the fiber lamina and were most likely myonuclei. The number of fibers containing morphologically abnormal nuclei was also significantly greater in suspended compared with control rats. Combined treatment with growth hormone and insulin-like growth factor I (GH/IGF-I) and resistance exercise attenuated the increase in TDT-positive nuclei (similar to 26%, P > 0.05) and significantly decreased the number of fibers with morphologically abnormal nuclei. The data suggest that 1) ''programmed nuclear death'' contributes to the elimination of myonuclei and/or satellite cells from atrophying fibers, and 2) GH/IGF-I administration plus muscle loading ameliorates the apoptosis associated with hindlimb unloading.