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细胞凋亡前期和凋亡细胞中线粒体的肿胀和初始外膜破裂。

Mitochondrial swelling and incipient outer membrane rupture in preapoptotic and apoptotic cells.

机构信息

Setor de Biologia Estrutural, Laboratório de Imunopatologia, Instituto de Medicina Tropical, Universidade de São Paulo, São Paulo, Brazil.

出版信息

Anat Rec (Hoboken). 2012 Oct;295(10):1647-59. doi: 10.1002/ar.22553. Epub 2012 Aug 21.

DOI:10.1002/ar.22553
PMID:22907871
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3549475/
Abstract

Outer mitochondrial membrane (OMM) rupture was first noted in isolated mitochondria in which the inner mitochondrial membrane (IMM) had lost its selective permeability. This phenomenon referred to as mitochondrial permeability transition (MPT) refers to a permeabilized inner membrane that originates a large swelling in the mitochondrial matrix, which distends the outer membrane until it ruptures. Here, we have expanded previous electron microscopic observations that in apoptotic cells, OMM rupture is not caused by a membrane stretching promoted by a markedly swollen matrix. It is shown that the widths of the ruptured regions of the OMM vary from 6 to 250 nm. Independent of the perforation size, herniation of the mitochondrial matrix appeared to have resulted in pushing the IMM through the perforation. A large, long focal herniation of the mitochondrial matrix, covered with the IMM, was associated with a rupture of the OMM that was as small as 6 nm. Contextually, the collapse of the selective permeability of the IMM may precede or follow the release of the mitochondrial proteins of the intermembrane space into the cytoplasm. When the MPT is a late event, exit of the intermembrane space proteins to the cytoplasm is unimpeded and occurs through channels that transverse the outer membrane, because so far, the inner membrane is impermeable. No channel within the outer membrane can expose to the cytoplasm a permeable inner membrane, because it would serve as a conduit for local herniation of the mitochondrial matrix.

摘要

外膜线粒体(OMM)破裂首先在失去选择性通透性的线粒体内膜(IMM)的分离线粒体中被注意到。这种现象被称为线粒体通透性转变(MPT),指的是通透性增加的内膜起源于线粒体基质的巨大肿胀,使外膜膨胀直至破裂。在这里,我们扩展了先前的电子显微镜观察结果,即在凋亡细胞中,OMM 破裂不是由明显肿胀的基质促进的膜拉伸引起的。结果表明,OMM 破裂区域的宽度从 6 至 250nm 不等。独立于穿孔的大小,线粒体基质的突出似乎导致 IMM 通过穿孔被推出。覆盖 IMM 的线粒体基质的大、长焦点突出与 OMM 的破裂有关,其破裂小至 6nm。从上下文来看,IMM 的选择性通透性的崩溃可能先于或后于线粒体膜间空间蛋白质向细胞质的释放。当 MPT 是一个晚期事件时,膜间空间蛋白质向细胞质的释放不受阻碍,并且通过穿过外膜的通道发生,因为到目前为止,内膜是不可渗透的。没有外膜内的通道可以将通透性的内膜暴露给细胞质,因为它将充当线粒体基质局部突出的导管。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/10666597a653/ar0295-1647-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/7fc2ad6db425/ar0295-1647-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/cf70a1981d17/ar0295-1647-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/d067e9f00b2f/ar0295-1647-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/e16f13eb9e09/ar0295-1647-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/5a82ef848a77/ar0295-1647-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/188526172c83/ar0295-1647-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/10666597a653/ar0295-1647-f9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/7fc2ad6db425/ar0295-1647-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/e73140bd008f/ar0295-1647-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/9af521eb4bb8/ar0295-1647-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/cf70a1981d17/ar0295-1647-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/d067e9f00b2f/ar0295-1647-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/e16f13eb9e09/ar0295-1647-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/5a82ef848a77/ar0295-1647-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/188526172c83/ar0295-1647-f8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/023c/3549475/10666597a653/ar0295-1647-f9.jpg

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