No change in myonuclear number during muscle unloading and reloading

No change in myonuclear number during muscle unloading and reloading
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DOI:
10.1152/japplphysiol.00436.2012
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发表时间:
2012-07-01
影响因子:
3.3
通讯作者:
Gundersen, K.
Gundersen, K.
中科院分区:
医学2区
文献类型:
--
作者:
Bruusgaard, J. C.;Egner, I. M.;Gundersen, K.

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[10]张文辉,张文辉.在肌肉卸载和重新加载期间,肌细胞数量没有变化。J Appl Physiol 113:290 - 296,2012.首次发表于2012年5月10日; doi:10.1152/japplphysiol.00436.2012.肌纤维是体内体积最大的细胞,它们具有多个细胞核,服务于细胞质的不同区域。大量的先前文献表明,后肢悬吊引起的萎缩通过细胞凋亡导致"过多"的肌核丢失。我们在这里证明,后肢悬吊引起的萎缩不会导致肌细胞核的损失,尽管在肌肉组织内的其他类型的细胞核的凋亡活性的强烈增加。因此,后肢悬吊与其他萎缩模型(如去神经支配、神经冲动阻滞和拮抗剂消融)相似。我们讨论了如何不同的结果,各种研究可以归因于分离肌细胞核从其他核的困难,并正常和卸载肌肉之间的被动特性的系统差异。在重新加载期间,后肢悬吊后,观察到放射状再生长,据信这伴随着从卫星细胞募集新的肌核。然而,在卸载过程中缺乏核损失使这些发现受到质疑。我们观察到,重新加载导致横截面积增加59%,纤维尺寸完全恢复到预悬浮水平。尽管有这种显著的增长,但肌核数量没有增加。因此,放射状再生长似乎不同于从头肥大,因为核仅在后者期间添加。我们推测,肌核的数量可能反映了肌纤维在其先前历史中的最大尺寸。
Bruusgaard JC, Egner IM, Larsen TK, Dupre-Aucouturier S, Desplanches D, Gundersen K. No change in myonuclear number during muscle unloading and reloading. J Appl Physiol 113: 290-296, 2012. First published May 10, 2012; doi: 10.1152/japplphysiol.00436.2012.Muscle fibers are the cells in the body with the largest volume, and they have multiple nuclei serving different domains of cytoplasm. A large body of previous literature has suggested that atrophy induced by hindlimb suspension leads to a loss of "excessive" myonuclei by apoptosis. We demonstrate here that atrophy induced by hindlimb suspension does not lead to loss of myonuclei despite a strong increase in apoptotic activity of other types of nuclei within the muscle tissue. Thus hindlimb suspension turns out to be similar to other atrophy models such as denervation, nerve impulse block, and antagonist ablation. We discuss how the different outcome of various studies can be attributed to difficulties in separating myonuclei from other nuclei, and to systematic differences in passive properties between normal and unloaded muscles. During reload, after hindlimb suspension, a radial regrowth is observed, which has been believed to be accompanied by recruitment of new myonuclei from satellite cells. The lack of nuclear loss during unloading, however, puts these findings into question. We observed that reload led to an increase in cross sectional area of 59%, and fiber size was completely restored to the presuspension levels. Despite this notable growth there was no increase in the number of myonuclei. Thus radial regrowth seems to differ from de novo hypertrophy in that nuclei are only added during the latter. We speculate that the number of myonuclei might reflect the largest size the muscle fibers have had in its previous history.