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Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model
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 proce...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5223200/ https://www.ncbi.nlm.nih.gov/pubmed/28071664 http://dx.doi.org/10.1038/srep39948 |
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author | Yu, Houyou Yang, Changwei Chen, Shi Huang, Yang Liu, Chuanming Liu, Jian Yin, Wen |
author_facet | Yu, Houyou Yang, Changwei Chen, Shi Huang, Yang Liu, Chuanming Liu, Jian Yin, Wen |
author_sort | Yu, Houyou |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-5223200 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52232002017-01-17 Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model Yu, Houyou Yang, Changwei Chen, Shi Huang, Yang Liu, Chuanming Liu, Jian Yin, Wen Sci Rep Article 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. Nature Publishing Group 2017-01-10 /pmc/articles/PMC5223200/ /pubmed/28071664 http://dx.doi.org/10.1038/srep39948 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Yu, Houyou Yang, Changwei Chen, Shi Huang, Yang Liu, Chuanming Liu, Jian Yin, Wen Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title | Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title_full | Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title_fullStr | Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title_full_unstemmed | Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title_short | Comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat Alzheimer’s disease and the cerebral ischemia model |
title_sort | comparison of the glycopattern alterations of mitochondrial proteins in cerebral cortex between rat alzheimer’s disease and the cerebral ischemia model |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5223200/ https://www.ncbi.nlm.nih.gov/pubmed/28071664 http://dx.doi.org/10.1038/srep39948 |
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