Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis.
Repair of injured plasma membrane by rapid Ca2+-dependent endocytosis.
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DOI：
10.1083/jcb.200708010
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发表时间：
2008-03-10
期刊：
影响因子：
--
通讯作者：
Andrews NW
中科院分区：
文献类型：
--
作者：
Idone V;Tam C;Goss JW;Toomre D;Pypaert M;Andrews NW
通过质膜损伤的Ca 2+内流触发快速修复过程，该过程先前显示需要溶酶体细胞器的胞吐作用（Reddy，A.，E. Caler和N.安德鲁斯2001. Cell. 106：157-169）。然而，胞吐作用如何导致膜重新密封仍然不清楚，特别是对于由成孔蛋白引起的稳定病变。在这项研究中，我们表明，Ca 2+依赖性resealing透化后的细菌毒素链球菌溶血素O（SLO）需要内吞作用通过一种新的途径，去除SLO含有孔从质膜。我们还发现，内吞作用同样需要修复损伤形成的机械损伤细胞。抑制病变的内吞作用（通过甾醇耗竭）抑制修复，而通过破坏肌动蛋白细胞骨架增强内吞作用有利于重新密封。因此，内吞作用通过从质膜去除损伤促进伤口重新密封。这些发现为细胞如何保护自己不仅免受机械损伤，而且免受免疫系统产生的微生物毒素和成孔蛋白的影响提供了重要的新见解。
Ca2+ influx through plasma membrane lesions triggers a rapid repair process that was previously shown to require the exocytosis of lysosomal organelles (Reddy, A., E. Caler, and N. Andrews. 2001. Cell. 106:157–169). However, how exocytosis leads to membrane resealing has remained obscure, particularly for stable lesions caused by pore-forming proteins. In this study, we show that Ca2+-dependent resealing after permeabilization with the bacterial toxin streptolysin O (SLO) requires endocytosis via a novel pathway that removes SLO-containing pores from the plasma membrane. We also find that endocytosis is similarly required to repair lesions formed in mechanically wounded cells. Inhibition of lesion endocytosis (by sterol depletion) inhibits repair, whereas enhancement of endocytosis through disruption of the actin cytoskeleton facilitates resealing. Thus, endocytosis promotes wound resealing by removing lesions from the plasma membrane. These findings provide an important new insight into how cells protect themselves not only from mechanical injury but also from microbial toxins and pore-forming proteins produced by the immune system.
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影响因子：
4.1
作者：
MORGAN, BP;CAMPBELL, AK
通讯作者：
CAMPBELL, AK
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作者：
Keefe, D;Shi, LF;Lieberman, J
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Lieberman, J
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Reddy, A;Caler, EV;Andrews, NW
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Andrews, NW
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作者：
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Steinhardt, RA
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作者：
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通讯作者：
Brostrom, MA