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强迫性热中风导致长期的骨肌肉表观遗传重编程,改变基因表达和小鼠卫星细胞功能受损
Kevin O Murray1, Jason O Brant2,3, Ray A Spradlin1
1Department of Applied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, Florida, United States.
概括
强迫性热中风 (EHS) 导致老鼠骨肌的长期分子和功能变化,降低了弹性. 这包括改变肌肉敏感性和抑制卫星细胞功能,表明可能对肌肉产生长期EHS影响.
科学领域:
- 运动生理学 运动生理学
- 肌肉生物学 肌肉生物学
- 环境压力生理学环境压力生理学
背景情况:
- 强迫性热中风 (EHS) 对骨肌肉的影响尚未完全理解.
- 肌肉软弱是EHS早期症状,但长期肌肉弹性变化尚不清楚.
- 之前的研究表明,四肢肌肉容易受到重复的EHS暴露.
研究的目的:
- 为了研究EHS诱导的骨肌肉弹性下降的分子起源.
- 为了评估肢体肌肉在EHS后的长期功能和分子变化.
- 评估EHS之后的卫星细胞功能和表观遗传修饰.
主要方法:
- 雌性小鼠接受了EHS (高温跑步) 或运动控制 (EXC).
- 在恢复1个月后评估肌肉特异力,咖啡因诱导的收缩,转录组和DNA甲基组.
- 评估了初级卫星细胞的增殖和分化能力.
主要成果:
- 肌肉显示咖啡因敏感性降低;没有观察到力量差异.
- 胃半腹肌表现出改变的基因表达 (缓慢的纤维,热冲击蛋白,肌体发生).
- 确定了大约2500个不同的甲基化DNA区域;卫星细胞显示抑制的增殖,但正常的分化.
结论:
- 骨肌肉在EHS1个月后表现出长期的分子和功能变化.
- 这些变化,包括咖啡因敏感性变化和卫星细胞增殖抑制,可能导致肌肉弹性降低.
- 骨肌可能是易受长期EHS影响的脆弱组织,类似于其他器官.
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