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

被引:13
|
作者
Yu, Houyou [1 ]
Yang, Changwei [1 ]
Chen, Shi [1 ]
Huang, Yang [1 ]
Liu, Chuanming [1 ]
Liu, Jian [1 ]
Yin, Wen [1 ]
机构
[1] Fourth Mil Med Univ, Xijing Hosp, Dept Emergency Med, Xian 710032, Peoples R China
来源
SCIENTIFIC REPORTS | 2017年 / 7卷
关键词
OXIDATIVE STRESS; BRAIN; DYSFUNCTION; GLYCOSYLATION; NEURONS; ROLES; DEATH; CELLS; DETERMINANTS; MECHANISMS;
D O I
10.1038/srep39948
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
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.
引用
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页数:13
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