细胞核作为组织损伤诱导的炎症的机制传感器
Balázs Enyedi1, Mark Jelcic1, Philipp Niethammer1
1Cell Biology Program, Memorial Sloan Kettering Cancer Center, New York, NY 10065, USA.
Cell
|May 21, 2016
概括
组织损伤引发细胞胀,通过核膜张力激活脂酶A2 (cPLA2). 这一过程通过释放酸 (AA) 和产生促炎信号来启动炎症.
科学领域:
- 细胞生物学 细胞生物学
- 炎症研究的研究.
- 机械生物学 机械生物学
背景情况:
- 组织损伤会引发炎症反应.
- 细胞基酸酶A2 (cPLA2) 释放了用于eicosanoid生产的阿拉基酸 (AA).
- 感知组织损伤激活cPLA2的机制尚不清楚.
研究的目的:
- 阐明组织损伤激活cPLA2.2的机制.
- 研究核在炎症期间感知机械应力的作用.
主要方法:
- 受伤的斑马鱼幼虫的现场成像.
- 研究cPLA2转位在对透细胞和核胀的反应中.
- 在孤立的核中复制cPLA2转位.
主要成果:
- 伤害导致透细胞胀和eicosanoid信号生成.
- 细胞和细胞核的透性胀通过转移到核外激活cPLA2.
- 核胀,而不仅仅是Ca2+升高,对于cPLA2转位至关重要.
- cPLA2转位是一个由核外张力驱动的物理过程.
结论:
- 核在炎症中充当机械传感器.
- 细胞胀和溶解被转化为促炎性eicosanoid信号.
- 核膜张力介于组织损伤后cPLA2的激活.
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