Skeletal muscle has the intrinsic ability to self-repair through a multifactorial process, but many aspects of its cellular and molecular mechanisms are not fully understood. There is increasing evidence that some members of the mammalian β-galactoside-binding protein family (galectins) are involved in the muscular repair process (MRP), including galectin-3 (Gal-3). However, there are many questions about the role of this protein on muscle self-repair. Here, we demonstrate that endogenous Gal-3 is required for: i) muscle repair in vivo using a chloride-barium myolesion mouse model, and ii) mouse primary myoblasts myogenic programming. Injured muscle from Gal-3 knockout mice (GAL3KO) showed persistent inflammation associated with compromised muscle repair and the formation of fibrotic tissue on the lesion site. In GAL3KO mice, osteopontin expression remained high even after 7 and 14 days of the myolesion, while MyoD and myogenin had decreased their expression. In GAL3KO mouse primary myoblast cell culture, Pax7 detection seems to sustain even when cells are stimulated to differentiation and MyoD expression is drastically reduced. The detection and temporal expression levels of these transcriptional factors appear to be altered in Gal-3-deficient myoblast. Gal-3 expression in WT states, both in vivo and in vitro, in sarcoplasm/cytoplasm and myonuclei; as differentiation proceeds, Gal-3 expression is drastically reduced, and its location is confined to the sarcolemma/plasma cell membrane. We also observed a change in the temporal–spatial profile of Gal-3 expression and muscle transcription factors levels during the myolesion. Overall, these results demonstrate that endogenous Gal-3 is required for the skeletal muscle repair process.

中文翻译：

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骨骼肌修复需要内源性 Galectin-3

骨骼肌具有通过多因素过程进行自我修复的内在能力，但其细胞和分子机制的许多方面尚不完全清楚。越来越多的证据表明，哺乳动物 β-半乳糖苷结合蛋白家族（半乳糖凝集素）的一些成员参与了肌肉修复过程（MRP），包括半乳糖凝集素 3（Gal-3）。然而，关于这种蛋白质对肌肉自我修复的作用存在许多疑问。在这里，我们证明了内源性 Gal-3 是必需的：i) 使用氯化钡肌瘤小鼠模型进行体内肌肉修复，以及 ii) 小鼠原代成肌细胞肌源性编程。来自 Gal-3 敲除小鼠 (GAL3KO) 的受伤肌肉显示出与肌肉修复受损和病变部位纤维化组织形成相关的持续炎症。在 GAL3KO 小鼠中，即使在肌瘤发生 7 天和 14 天后，骨桥蛋白的表达仍然很高，而 MyoD 和肌细胞生成素的表达降低了。在 GAL3KO 小鼠原代成肌细胞培养物中，Pax7 检测似乎可以维持，即使当细胞被刺激分化并且 MyoD 表达显着降低时也是如此。这些转录因子的检测和时间表达水平似乎在 Gal-3 缺陷型成肌细胞中发生了改变。Gal-3 在 WT 状态下的表达，在体内和体外，在肌浆/细胞质和肌核中；随着分化的进行，Gal-3 的表达急剧下降，其位置仅限于肌膜/浆细胞膜。我们还观察到在肌裂期间 Gal-3 表达和肌肉转录因子水平的时空分布的变化。全面的，