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Physical training modulates structural and functional features of cell nuclei in type II myofibers of old mice.

机译:体能训练可调节老小鼠II型肌纤维中细胞核的结构和功能特征。

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Aging is associated with a progressive loss of muscle mass, strength, and function, a condition known as sarcopenia, which represents an important risk factor for physical disability in elderly. The mechanisms leading to sarcopenia are still largely unknown, and no specific therapy is presently available to counteract its onset or progress. Many studies have stressed the importance of physical exercise as an effective approach to prevent/limit the age-related muscle mass loss. This study investigated the effects of physical training on pre-mRNA pathways in quadriceps and gastrocnemius muscles of old mice by ultrastructural cytochemistry: Structural and in situ molecular features of myonuclei and satellite cell nuclei of type II fibers were compared in exercised versus sedentary old mice, using adult individuals as control. Our results demonstrated that in myonuclei of old mice physical exercise stimulates pre-mRNA transcription, splicing, and export to the cytoplasm, likely increasing muscle protein turnover. In satellite cells, the effect of physical exercise seems to be limited to the reactivation of some factors involved in the transcriptional and splicing apparatus without increasing RNA production, probably making these quiescent cells more responsive to activating stimuli.
机译:衰老与肌肉质量,力量和功能的逐步丧失有关,这种状态称为肌肉减少症,它代表老年人身体残疾的重要危险因素。导致肌肉减少症的机制仍是很大程度上未知的,并且目前没有可用于抵消其发作或进展的特异性疗法。许多研究强调体育锻炼作为预防/限制与年龄有关的肌肉质量流失的有效方法的重要性。这项研究通过超微结构细胞化学研究了体育锻炼对老年小鼠股四头肌和腓肠肌前mRNA途径的影响:比较了运动型和久坐型老年小鼠的肌核和II型纤维卫星细胞核的结构和原位分子特征,以成年个体为对照。我们的研究结果表明,在老年小鼠的肌核中,体育锻炼会刺激mRNA之前的转录,剪接并输出到细胞质,这可能会增加肌肉蛋白质的更新。在卫星细胞中,体育锻炼的作用似乎仅限于重新激活转录和剪接设备中涉及的某些因素,而不会增加RNA的产生,这可能会使这些静态细胞对激活刺激更加敏感。

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