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哇巴因诱导的细胞质囊泡及其在细胞容积维持中的作用。

Ouabain-induced cytoplasmic vesicles and their role in cell volume maintenance.

作者信息

Russo M A, Morgante E, Russo A, van Rossum G D, Tafani M

机构信息

Laboratory of Molecular and Cellular Pathology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Roma, Italy.

Department of Experimental Medicine, Sapienza University of Rome, 00161 Rome, Italy.

出版信息

Biomed Res Int. 2015;2015:487256. doi: 10.1155/2015/487256. Epub 2015 Mar 19.

DOI:10.1155/2015/487256
PMID:25866786
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4383472/
Abstract

Cellular swelling is controlled by an active mechanism of cell volume regulation driven by a Na(+)/K(+)-dependent ATPase and by aquaporins which translocate water along the osmotic gradient. Na(+)/K(+)-pump may be blocked by ouabain, a digitalic derivative, by inhibition of ATP, or by drastic ion alterations of extracellular fluid. However, it has been observed that some tissues are still able to control their volume despite the presence of ouabain, suggesting the existence of other mechanisms of cell volume control. In 1977, by correlating electron microscopy observation with ion and water composition of liver slices incubated in different metabolic conditions in the presence or absence of ouabain, we observed that hepatocytes were able to control their volume extruding water and recovering ion composition in the presence of ouabain. In particular, hepatocytes were able to sequester ions and water in intracellular vesicles and then secrete them at the bile canaliculus pole. We named this "vesicular mechanism of cell volume control." Afterward, this mechanism has been confirmed by us and other laboratories in several mammalian tissues. This review summarizes evidences regarding this mechanism, problems that are still pending, and questions that need to be answered. Finally, we shortly review the importance of cell volume control in some human pathological conditions.

摘要

细胞肿胀受细胞体积调节的主动机制控制,该机制由钠钾依赖的ATP酶以及沿渗透梯度转运水的水通道蛋白驱动。钠钾泵可能会被哇巴因(一种洋地黄衍生物)、ATP抑制或细胞外液的剧烈离子变化所阻断。然而,已经观察到一些组织在存在哇巴因的情况下仍能够控制其体积,这表明存在其他细胞体积控制机制。1977年,通过将电子显微镜观察结果与在不同代谢条件下、存在或不存在哇巴因的情况下孵育的肝切片的离子和水成分相关联,我们观察到肝细胞在存在哇巴因的情况下能够通过排出水分和恢复离子成分来控制其体积。特别是,肝细胞能够将离子和水隔离在细胞内囊泡中,然后在胆小管极分泌它们。我们将此命名为“细胞体积控制的囊泡机制”。此后,我们和其他实验室在几种哺乳动物组织中证实了这一机制。这篇综述总结了关于该机制的证据、仍未解决的问题以及需要回答的疑问。最后,我们简要回顾了细胞体积控制在一些人类病理状况中的重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef02/4383472/498a41807c37/BMRI2015-487256.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef02/4383472/a11081a3d294/BMRI2015-487256.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef02/4383472/498a41807c37/BMRI2015-487256.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef02/4383472/a11081a3d294/BMRI2015-487256.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef02/4383472/498a41807c37/BMRI2015-487256.003.jpg

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