在附着结处先前存在的组织机械高血压会扰乱表皮质中的阿波托斯挤出
Zoya Mann1, Fayth Lim1, Suzie Verma1
1Division of Cell and Developmental Biology, Institute for Molecular Bioscience, The University of Queensland, Brisbane, Australia 4072.
皮质细胞通过尖端挤出消除受损细胞. 增加的机械张力会破坏这个过程,导致细胞被保留,并可能导致炎症.
科学领域:
- 细胞生物学 细胞生物学
- 生物物理学的生物物理.
- 组织力学 组织力学
背景情况:
- 角膜挤出是表皮平衡的关键过程,它去除了质细胞,以保持屏障的完整性和预防炎症.
- 这一过程涉及到活性力学,机械传导和局部组织特性调制.
研究的目的:
- 调查先前在粘附结 (AJs) 处存在的机械张力在调节阿波托斯挤出效率中的作用.
- 为了确定与炎症相关的因素如何通过机械途径影响apoptotic挤出.
主要方法:
- 过度表达一种相模拟性Myosin II调节光链 (MRLC),以增加机械张力.
- 用益炎性细胞因子TNFα治疗以模仿炎症状况.
- 利用抑制性MRLC突变物和热胺抑制剂来逆转机械张力.
主要成果:
- 由MRLC过度表达引起的AJs的基线机械张力增加,损害了apoptotic挤出.
- 激发TNFα会增加Myosin II活性和AJ张力,扰乱细胞缩挤出并导致细胞保留.
- 逆转机械张力在药理上恢复了TNFα处理的表皮质中的apoptotic挤出.
结论:
- 基线组织张力是透性挤出疗效的关键决定因素.
- 像TNFα这样的致病性因素可以利用机械张力来破坏表皮细胞对亡的恒常反应.
- 调节组织张力为涉及上皮功能障碍的炎症状况提供了潜在的治疗策略.
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