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首页> 外文期刊>American Journal of Physiology >Roles of IL-1α/β in regeneration of cardiotoxin-injured muscle and satellite cell function
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Roles of IL-1α/β in regeneration of cardiotoxin-injured muscle and satellite cell function

机译：IL-1α/β在心脏毒素损伤肌肉和卫星电池功能再生中的作用

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Skeletal muscle regeneration after injury is a complex process involving interactions between inflammatory microenvironments and satellite cells. Interleukin (IL)-1 is a key mediator of inflammatory responses and exerts pleiotropic impacts on various cell types. Thus, we aimed to investigate the role of IL-1 during skeletal muscle regeneration. We herein show that IL-1α/β-double knockout (IL-1KO) mice exhibit delayed muscle regeneration after cardiotoxin (CTX) injection, characterized by delayed infiltrations of immune cells accompanied by suppressed local production of proinflammatory factors including IL-6 and delayed increase of paired box 7 (PAX7)-positive satellite cells postinjury compared with those of wild-type (WT) mice. A series of in vitro experiments using satellite cells obtained from the IL-1KO mice unexpectedly revealed that IL-1KO myoblasts have impairments in terms of both proliferation and differentiation, both of which were reversed by exogenous IL-1β administration in culture. Intriguingly, the delay in myogenesis was not attributable to the myogenic transcriptional program since MyoD and myogenin were highly upregulated in IL-1KO cells, instead appearing, at least in part, to be due to dysregulation of cellular fusion events, possibly resulting from aberrant actin regulatory systems. We conclude that IL-1 plays a positive role in muscle regeneration by coordinating the initial interactions among inflammatory microenvironments and satellite cells. Our findings also provide compelling evidence that IL-1 is intimately engaged in regulating the fundamental function of myocytes.
机译：损伤后的骨骼肌再生是涉及炎症微环境和卫星细胞之间的相互作用的复杂过程。白细胞介素（IL）-1是炎症反应的关键介质，并对各种细胞类型发挥肺炎的影响。因此，我们旨在探讨IL-1在骨骼肌再生期间的作用。我们在此表明​​，IL-1α/β - 双敲除（IL-1KO）小鼠在心脏毒素（CTX）注射后表现出延迟肌肉再生，其特征在于免疫细胞的延迟渗透，伴随局部产生的临床炎症因子，包括IL-6并延迟与野生型（WT）小鼠相比，将配对盒7（PAX7）阳性卫星细胞增加。一系列使用从IL-1KO小鼠获得的卫星细胞的体外实验意外地揭示了IL-1KO肌细胞在增殖和分化方面具有损伤，这两者都被外源IL-1β培养给药逆转。有趣的是，由于Myod和Myogenin在IL-1KO细胞中高度上调，因此，由于在IL-1KO细胞中高度上调，因此，Mycocerescesis的延迟不归因于肌原素转录程序，而是由于细胞融合事件的失衡而出现，可能是由异常肌动蛋白引起的监管系统。我们得出结论，通过协调炎性微环境和卫星细胞的初始相互作用，IL-1在肌肉再生中起着积极作用。我们的调查结果还提供了令人信服的证据，即IL-1密切地从事调节肌细胞的根本功能。

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