附着细胞经历了由actomyosin动力学介导的速度软化
Samuel F Boland1, Juan E Abrahante2, Patrick W Alford1
1Department of Biomedical Engineering, University of Minnesota, Minneapolis, Minnesota.
在受伤期间,细胞表现出依赖于速率的机械软化,这种软化是由actin-myosin动态介导的. 这种保护机制在高应变率下失败,可能导致身体创伤后的慢性疾病.
科学领域:
- 细胞力学 细胞力学
- 生物物理学的生物物理.
- 生物材料科学是生物材料的科学.
背景情况:
- 慢性疾病可能源于身体创伤和细胞变形.
- 细胞对损伤的机械反应,特别是高应变率,仍然不清楚.
研究的目的:
- 研究血管光滑肌细胞的依赖应变率的机械行为.
- 了解对生理和超生理变形速率的反应背后的细胞机制.
主要方法:
- 研究了血管光滑肌肉细胞在五个数量级的应变率.
- 在张力和卸载过程中分析了细胞力学.
- 检查了actin-myosin结合动学的作用.
主要成果:
- 细胞表现出显著的速度软化在张力随着增长的应变率.
- 当细胞恢复到零应变 (可逆) 时,没有观察到速率依赖.
- 超生理应变率破坏了收缩力,并通过actin-myosin结合改变了基因表达.
结论:
- 动氨酸-肌氨酸结合动态调解可逆速率软化,这是细胞自我保护机制.
- 这种细胞骨放松机制在高应变率下失效,增加了脆弱性.
- 在高应变率下,受损的细胞力学可能会将身体创伤与疾病联系起来.
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