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首页> 外文期刊>Aging cell. >miR-24 and its target gene Prdx6 regulate viability and senescence of myogenic progenitors during aging
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miR-24 and its target gene Prdx6 regulate viability and senescence of myogenic progenitors during aging

机译：MiR-24及其靶基因PRDX6在老化期间调节肌原血管祖的活力和衰老

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Satellite cell-dependent skeletal muscle regeneration declines during aging. Disruptions within the satellite cells and their niche, together with alterations in the myofibrillar environment, contribute to age-related dysfunction and defective muscle regeneration. In this study, we demonstrated an age-related decline in satellite cell viability and myogenic potential and an increase in ROS and cellular senescence. We detected a transient upregulation of miR-24 in regenerating muscle from adult mice and downregulation of miR-24 during muscle regeneration in old mice. FACS-sorted satellite cells were characterized by decreased levels of miR-24 and a concomitant increase in expression of its target: Prdx6. Using GFP reporter constructs, we demonstrated that miR-24 directly binds to its predicted site within Prdx6?mRNA. Subtle changes in Prdx6?levels following changes in miR-24 expression indicate miR-24 plays a role in fine-tuning Prdx6 expression. Changes in miR-24 and Prdx6?levels were associated with altered mitochondrial ROS generation, increase in the DNA damage marker: phosphorylated-H2Ax and changes in viability, senescence, and myogenic potential of myogenic progenitors from mice and humans. The effects of miR-24 were more pronounced in myogenic progenitors from old mice, suggesting a context-dependent role of miR-24 in these cells, with miR-24 downregulation likely a part of a compensatory response to declining satellite cell function during aging. We propose that downregulation of miR-24 and subsequent upregulation of Prdx6 in muscle of old mice following injury are an adaptive response to aging, to maintain satellite cell viability and myogenic potential through regulation of mitochondrial ROS and DNA damage pathways.
机译：老化期间卫星细胞依赖性骨骼肌再生下降。卫星细胞和它们的利基中的破坏以及肌原纤维环境的改变，有助于年龄相关的功能障碍和缺陷的肌肉再生。在这项研究中，我们展示了卫星细胞活力和肌原潜力的年龄相关的下降，以及ROS和细胞衰老的增加。我们检测到MiR-24的瞬态上调，在成人小鼠中再生肌肉，并在旧小鼠的肌肉再生期间的miR-24下调。 FACS - 分选卫星卫星细胞的特征在于miR-24的水平降低，并且伴随其靶标的表达的增加：PRDX6。使用GFP报告器构建体，我们证明MIR-24直接绑定到PRDX6内的预测部位？mRNA。 PRDX6的微妙变化？MIR-24表达式的更改后的水平表示MiR-24在微调PRDX6表达式中起作用。 MiR-24和PRDX6的变化与改变的线粒体ROS产生相关，DNA损伤标记的增加：磷酸化-H2AX和生存率，衰老和肌原血管祖从小鼠和人类的变化。 MiR-24的肌原素祖血管血小鼠血小鼠疗法更加明显，表明MIR-24在这些细胞中的上下文依赖性作用，MIR-24下调可能是对老化期间卫星电池功能下降的补偿性反应的一部分。我们提出，在损伤后，损伤后的旧小鼠的肌肉中的miR-24的下调和随后上调的prdx6是对老化的适应性反应，通过调节线粒体ROS和DNA损伤途径来维持卫星细胞活力和肌原潜力。

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