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比较大鼠阿尔茨海默病和脑缺血模型大脑皮质中线粒体蛋白糖基化模式的改变。

Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer's disease and the cerebral ischemia model.

机构信息

Department of Emergency Medicine, Xijing Hospital, the Fourth Military Medical University, Xi'an, 710032, China.

出版信息

Sci Rep. 2017 Jan 10;7:39948. doi: 10.1038/srep39948.

DOI:10.1038/srep39948
PMID:28071664
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5223200/
Abstract

Alzheimer's disease (AD) and ischemic brain injury are two major neurodegenerative diseases. Mitochondrial dysfunction commonly occurs in AD and ischemic brain injury. Currently, little attention has been paid to the glycans on mitochondrial glycoproteins, which may play vital roles during the process of mitochondrial dysfunction. The aim of this study was to illustrate and compare the glycopattern alterations of mitochondrial glycoproteins extracted from the cerebral cortex of the rat models of these two diseases using High-throughput lectin microarrays. The results shown that the number of lectins with significant differences compared to normal brains was nine for the rat sporadic Alzheimer's disease (SAD) model and eighteen for the rat middle cerebral artery occlusion (MCAO) model. Interestingly, five lectins showed opposite expression patterns between the SAD and MCAO rat models. We conclude that glycopattern alterations of mitochondrial glycoproteins in the cerebral cortex may provide vital information to help understand mitochondrial dysfunction in AD and ischemic brain injury. In addition, glycans recognized by diverse lectins with opposite expression patterns between these two diseases hints at the different pathomechanisms of mitochondrial dysfunction in AD and ischemic brain injury.

摘要

阿尔茨海默病(AD)和缺血性脑损伤是两种主要的神经退行性疾病。线粒体功能障碍常见于 AD 和缺血性脑损伤。目前,人们对线粒体糖蛋白上的聚糖关注较少,而这些聚糖可能在线粒体功能障碍过程中发挥重要作用。本研究旨在使用高通量凝集素微阵列阐明和比较这两种疾病大鼠模型大脑皮质中提取的线粒体糖蛋白的糖型改变。结果表明,与正常大脑相比,散发性 AD 大鼠模型有 9 种凝集素有显著差异,大脑中动脉闭塞(MCAO)大鼠模型有 18 种。有趣的是,有 5 种凝集素在 SAD 和 MCAO 大鼠模型之间表现出相反的表达模式。我们得出结论,大脑皮质中线粒体糖蛋白的糖型改变可能为帮助理解 AD 和缺血性脑损伤中的线粒体功能障碍提供重要信息。此外,这两种疾病之间具有相反表达模式的不同凝集素识别的聚糖提示 AD 和缺血性脑损伤中线粒体功能障碍的不同发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/a1b13e87f629/srep39948-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/827fff9eada4/srep39948-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/45d262c98afe/srep39948-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/4c811f3a3da2/srep39948-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/cdb7d80a6efd/srep39948-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/92608d27a798/srep39948-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/76784f3c164f/srep39948-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/a1b13e87f629/srep39948-f7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/827fff9eada4/srep39948-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/45d262c98afe/srep39948-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/4c811f3a3da2/srep39948-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/cdb7d80a6efd/srep39948-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/92608d27a798/srep39948-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/76784f3c164f/srep39948-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0432/5223200/a1b13e87f629/srep39948-f7.jpg

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