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诱导型 70kDa 热休克蛋白在小鼠中的过表达可改善萎缩骨骼肌的结构和功能恢复。

Overexpression of inducible 70-kDa heat shock protein in mouse improves structural and functional recovery of skeletal muscles from atrophy.

机构信息

Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Lineu Prestes Av. 2415, São Paulo, São Paulo, 05508-000, Brazil.

出版信息

Pflugers Arch. 2012 Apr;463(5):733-41. doi: 10.1007/s00424-012-1087-x. Epub 2012 Mar 6.

DOI:10.1007/s00424-012-1087-x
PMID:22391802
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3568507/
Abstract

Heat shock proteins play a key regulatory role in cellular defense. To investigate the role of the inducible 70-kDa heat shock protein (HSP70) in skeletal muscle atrophy and subsequent recovery, soleus (SOL) and extensor digitorum longus (EDL) muscles from overexpressing HSP70 transgenic mice were immobilized for 7 days and subsequently released from immobilization and evaluated after 7 days. Histological analysis showed that there was a decrease in cross-sectional area of type II myofiber from EDL and types I and II myofiber from SOL muscles at 7-day immobilization in both wild-type and HSP70 mice. At 7-day recovery, EDL and SOL myofibers from HSP70 mice, but not from wild-type mice, recovered their size. Muscle tetanic contraction decreased only in SOL muscles from wild-type mice at both 7-day immobilization and 7-day recovery; however, it was unaltered in the respective groups from HSP70 mice. Although no effect in a fatigue protocol was observed among groups, we noticed a better contractile performance of EDL muscles from overexpressing HSP70 groups as compared to their matched wild-type groups. The number of NCAM positive-satellite cells reduced after immobilization and recovery in both EDL and SOL muscles from wild-type mice, but it was unchanged in the muscles from HSP70 mice. These results suggest that HSP70 improves structural and functional recovery of skeletal muscle after disuse atrophy, and this effect might be associated with preservation of satellite cell amount.

摘要

热休克蛋白在细胞防御中发挥关键调节作用。为了研究诱导型 70kDa 热休克蛋白(HSP70)在骨骼肌萎缩及其随后恢复中的作用,将过表达 HSP70 的转基因小鼠的比目鱼肌(SOL)和趾长伸肌(EDL)固定 7 天,然后从固定中释放并在 7 天后进行评估。组织学分析显示,在野生型和 HSP70 小鼠的 EDL 和 SOL 肌肉中,II 型肌纤维的横截面积在 7 天固定时均减少。在 7 天恢复时,HSP70 小鼠的 EDL 和 SOL 肌纤维,但野生型小鼠的肌纤维没有恢复其大小。在 7 天固定和 7 天恢复时,仅在野生型小鼠的 SOL 肌肉中观察到肌肉强直收缩减少;然而,在 HSP70 小鼠的相应组中,其并未改变。尽管在疲劳方案中未观察到各组之间的影响,但我们注意到过表达 HSP70 的 EDL 肌肉的收缩性能优于其匹配的野生型组。在野生型小鼠的 EDL 和 SOL 肌肉中,固定和恢复后 NCAM 阳性卫星细胞的数量减少,但在 HSP70 小鼠的肌肉中未改变。这些结果表明,HSP70 可改善废用性萎缩后骨骼肌的结构和功能恢复,这种作用可能与卫星细胞数量的保存有关。

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