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连接蛋白43/47通道对于髓鞘形成和脱髓鞘过程中星形胶质细胞/少突胶质细胞的相互作用至关重要。

Connexin 43/47 channels are important for astrocyte/ oligodendrocyte cross-talk in myelination and demyelination.

作者信息

Basu Rahul, Sarma Jayasri DAS

机构信息

Department of Biological Sciences, Indian Institute of Science Education and Research Kolkata, Mohanpur 741246, India.

出版信息

J Biosci. 2018 Dec;43(5):1055-1068. doi: 10.1007/s12038-018-9811-0.

DOI:10.1007/s12038-018-9811-0
PMID:30541963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7091171/
Abstract

The gap junctions (GJs), which form intercellular communicating channels between two apposing cells or form hemichannel with extracellular environment, perform crucial functions to maintain small molecule homeostasis. The central nervous system (CNS) GJs are important for maintenance of myelin sheath and neuronal activity. Connexin (Cx) proteins are building blocks of GJs. Recent cell-biological investigations show that amongst the CNS specific Cxs, the most abundant Cx protein, Cx43 and its oligodendrocytic coupling partner Cx47 primarily important for maintenance of CNS myelin. Recent investigations elucidate that the expression of Cx43 and Cx47 is very important to maintain K? buffering and nutrient homeostasis in oligodendrocytes, CNS myelin and oligodendrocyte function. The investigations on Multiple Sclerosis (MS) patient samples and EAE hypothesized that the functional loss of Cx43/Cx47 could be associated with spread of chronic MS lesions. Exploring the mechanism of initial GJ alteration and its effect on demyelination in this model of MS might play a primary role to understand the basis of altered CNS homeostasis, observed during MS. In this review, we mainly discuss the role of CNS GJs, specifically the Cx43/Cx47 axis in the perspective of demyelination.

摘要

间隙连接(GJs)在两个相邻细胞之间形成细胞间通讯通道,或与细胞外环境形成半通道,在维持小分子内环境稳定方面发挥着关键作用。中枢神经系统(CNS)的间隙连接对于维持髓鞘和神经元活动很重要。连接蛋白(Cx)是间隙连接的组成成分。最近的细胞生物学研究表明,在中枢神经系统特异性连接蛋白中,最丰富的连接蛋白Cx43及其少突胶质细胞偶联伴侣Cx47对维持中枢神经系统髓鞘至关重要。最近的研究表明,Cx43和Cx47的表达对于维持少突胶质细胞、中枢神经系统髓鞘和少突胶质细胞功能中的钾缓冲和营养物质稳态非常重要。对多发性硬化症(MS)患者样本和实验性自身免疫性脑脊髓炎(EAE)的研究推测,Cx43/Cx47的功能丧失可能与慢性MS病变的扩散有关。在这种MS模型中探索间隙连接初始改变的机制及其对脱髓鞘的影响,可能在理解MS期间观察到的中枢神经系统内环境稳态改变的基础方面发挥主要作用。在这篇综述中,我们主要从中枢神经系统间隙连接的角度,特别是Cx43/Cx47轴在脱髓鞘中的作用进行讨论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/ff95ad482e48/12038_2018_9811_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/255b17f81939/12038_2018_9811_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/956287d0ebe5/12038_2018_9811_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/ff95ad482e48/12038_2018_9811_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/255b17f81939/12038_2018_9811_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/956287d0ebe5/12038_2018_9811_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d42/7091171/ff95ad482e48/12038_2018_9811_Fig3_HTML.jpg

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