Lack of galectin-1 results in defects in myoblast fusion and muscle regeneration
Lack of galectin-1 results in defects in myoblast fusion and muscle regeneration
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DOI：
10.1002/dvdy.21123
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发表时间：
2007-04-01
影响因子：
2.5
通讯作者：
Lawrence-Watt, Diana J.
中科院分区：
文献类型：
--
作者：
Georgiadis, Vasilios;Stewart, Helen J. S.;Lawrence-Watt, Diana J.
Galectin-1与骨骼肌的发育有关，在肌纤维形成时表达最强。此外，在外源性Galectin-1存在的情况下，单核成肌细胞在体外表现出更多的融合。在目前的研究中，我们使用Galectin-1缺失的小鼠来阐明Galectin-1在骨骼肌发育和再生中的作用。来自Galectin-1突变体的成肌细胞在体外融合能力降低。在Galectin-1缺失突变体中，有证据表明新生阶段的肌肉纤维发育延迟，与成年期的野生型相比，肌肉纤维直径变小。Galectin-1突变体的肌肉再生也受到了影响，这一过程被推迟，并保持了较小的纤维尺寸。因此，这些结果表明，Galectin-1在成肌细胞的体外、体内融合和诱导损伤恢复后的再生中发挥了明确的作用。
Galectin-1 has been implicated in the development of skeletal muscle, being maximally expressed at the time of myofiber formation. Furthermore, in the presence of exogenous galectin-1, mononuclear myoblasts show increased fusion in vitro. In the current study, we have used the galectin-1 null mouse to elucidate the role of galectin-1 in skeletal muscle development and regeneration. Myoblasts derived from the galectin-1 mutant showed a reduced ability to fuse in vitro. In galectin-1 null mutants, there was evidence of a delay in muscle fiber development at the neonatal stage and muscle fiber diameter was reduced when compared with wild-type at the adult stage. Muscle regeneration was also compromised in the galectin-1 mutant with the process being delayed and a reduced fiber size being maintained. These results, therefore, show a definitive role for galectin-1 in fusion of myoblasts both in vitro, in vivo, and in regeneration after recovery from induced injury.