AGE-RELATED DIFFERENCES IN REGENERATION OF DYSTROPHIC (MDX) AND NORMAL MUSCLE IN THE MOUSE

AGE-RELATED DIFFERENCES IN REGENERATION OF DYSTROPHIC (MDX) AND NORMAL MUSCLE IN THE MOUSE
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DOI:
10.1002/mus.880181011
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发表时间:
1995-10-01
期刊:
影响因子:
3.4
通讯作者:
SEBILLE, A
SEBILLE, A
中科院分区:
医学3区
文献类型:
--
作者:
PASTORET, C;SEBILLE, A

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mdx 小鼠是人类杜氏肌营养不良症 (DMD) 的遗传同源物,其骨骼肌再生能力更强。在这里,我们测试了以下假设:mdx 小鼠的肌肉比非营养不良动物的肌肉再生能力更好。我们在 mdx 和野生型 (C57BL/10) 小鼠中研究了 3 周和 2 个月时因趾长伸肌 (EDL) 去神经断血管损伤 (DD) 导致的肌肉再生,在 3 至 180 天后进行了肌肉再生的组织学和形态测量研究。当对 3 周龄的 C57BL/10 小鼠进行 DD 时, 再生纤维中的非外周细胞核在 3 个月内逐渐减少,这种减少在 2 个月时进行 DD 的动物中并未出现,表明在这两个年龄的小鼠的肌肉再生中动员了两种不同的肌肉前体细胞群。此外,mdx EDL 肌肉在术后 60 天的再生过程中与对照组相似,如平均直径和百分比的分布所示。 肌纤维的非外周核,术后60天后,mdx肌肉的坏死/再生特征再次出现,表明mdx再生的肌纤维仍然容易发生退化。 (C) 1995 约翰威利父子公司
The mdx mouse, a genetic homologue of human Duchenne muscular dystrophy (DMD), has been attributed with a greater regenerative capacity of its skeletal muscles, Here, we have tested the hypothesis that muscles of mdx mice regenerate better than those of nondystrophic animals. We studied muscle regeneration resulting from a denervation-devascularization injury (DD) of extensor digitorum longus muscle (EDL) at 3 weeks and 2 months in mdx and wild-type (C57BL/10) mice, Histological and morphometrical studies of muscle regeneration were made from 3 to 180 days later, When DD was performed in 3-week-old C57BL/10 mice, the percentages of nonperipheral nuclei in regenerated fibers decreased progressively over 3 months, This decrease did not occur in animals where DDs were performed at 2 months, suggesting that two different populations of muscle precursor cells are mobilized in muscle regeneration in mice at these two ages, Moreover, mdx EDL muscle regenerated similarly to the controls for up to 60 postoperative days, as shown by distribution of mean diameters and percentage of nonperipheral nuclei of muscle fibers, After 60 postoperative days, necrosis/regeneration characteristics of mdx muscles recurred, suggesting that mdx-regenerated muscle fibers remain susceptible to degeneration. (C) 1995 John Wiley & Sons, Inc.