Cellular adaptations in soleus muscle during recovery after hindlimb unloading
Cellular adaptations in soleus muscle during recovery after hindlimb unloading
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DOI：
10.1111/j.1748-1716.2007.01747.x
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发表时间：
2008-03-01
影响因子：
6.3
通讯作者：
Roy, R. R.
中科院分区：
文献类型：
--
作者：
Oishi, Y.;Ogata, T.;Roy, R. R.
目的：我们采用慢性卸载后再加载的模型来研究与比目鱼肌萎缩和随后恢复相关的凋亡反应。方法：雄性Wistar大鼠后肢卸荷2周，后肢卸荷0、3、7、14 d。一半重装hu的大鼠被给予环孢素A (CsA)，一种钙调磷酸酶（CaN）抑制剂。结果：HU治疗2周后，比目鱼肌纤维萎缩（73%），慢型I型纤维/肌球蛋白重链（MyHC）组成减少。未治疗的大鼠的纤维大小和I型MyHC组成在恢复第14天恢复到接近年龄匹配的对照水平，而csa治疗的大鼠则没有。与对照组相比，2周大鼠心肌核数减少，凋亡核数增加。在两个hu恢复组中，这些数值分别在恢复7天和14天后恢复到对照水平。HU治疗2周后，热休克蛋白（Hsp） 60和72、线粒体细胞色素c氧化酶亚基IV （Cox IV）和过氧化物酶体增殖物激活受体γ辅助激活因子1 （PGC-1）蛋白水平低于对照组。在笼内恢复期间，两组的所有这些蛋白水平均逐渐升高至或高于对照组水平。结论：我们的研究结果表明凋亡机制参与了慢性卸载和随后的再加载过程中mynuclear数的调节。此外，CaN似乎与纤维大小和表型适应有关，但与凋亡反应无关。
Aim: We used a model of chronic unloading followed by reloading to examine the apoptotic responses associated with soleus muscle atrophy and subsequent recovery.Methods: Male Wistar rats were subjected to hindlimb unloading (HU) for 2 weeks and subsequent reloading for 0, 3, 7 and 14 days. One-half of the HU-reloaded rats were administered cyclosporine A (CsA), a calcineurin (CaN) inhibitor.Results: There was fibre atrophy (73%) and a decrease in slow type I fibre/myosin heavy chain (MyHC) composition in the soleus muscle after 2 weeks of HU. Fibre size and type I MyHC composition recovered to near the age-matched control levels by recovery day 14 in non-treated, but not in CsA-treated, rats. Myonuclear number was lower and the number of apoptotic nuclei higher in 2-week HU than control rats. These values returned to control levels after 7 and 14 days of recovery, respectively, in both HU-recovery groups. After 2 weeks of HU, the levels of heat shock proteins (Hsp) 60 and 72, mitochondrial cytochrome c oxidase subunit IV (Cox IV), and peroxisome proliferator-activated receptor gamma coactivator 1 (PGC-1) proteins were lower than control. The levels of all of these proteins gradually increased to or above the control levels during cage recovery in both groups.Conclusion: Our results indicate that apoptotic mechanisms are involved in the modulation of myonuclear number during chronic unloading and subsequent reloading. Furthermore, it appears that CaN is related to fibre size and phenotype adaptations, but not to apoptotic responses.