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Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury
Aquaporin 4 (AQP4) is a widely distributed membrane protein, which is found in glial cells, ependymocytes and capillary endothelial cells in the brain, and particularly in the choroid plexus. AQP4 is a key regulator of water metabolism, and changes in its expression following brain injury are associ...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2015
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626127/ https://www.ncbi.nlm.nih.gov/pubmed/26459070 http://dx.doi.org/10.3892/mmr.2015.4372 |
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author | ZHANG, CHENGCHENG CHEN, JIANQIANG LU, HONG |
author_facet | ZHANG, CHENGCHENG CHEN, JIANQIANG LU, HONG |
author_sort | ZHANG, CHENGCHENG |
collection | PubMed |
description | Aquaporin 4 (AQP4) is a widely distributed membrane protein, which is found in glial cells, ependymocytes and capillary endothelial cells in the brain, and particularly in the choroid plexus. AQP4 is a key regulator of water metabolism, and changes in its expression following brain injury are associated with pathological changes in the damaged side of the brain; however, the effects of brain injury on AQP4 and injury-induced pathological changes in the contralateral non-damaged side of the brain remain to be fully elucidated. In the present study, male Sprague-Dawley rats were subjected to traumatic brain injury (TBI) and changes in brain water content, the expression of AQP4 expression and pathological characteristics in the damaged and contralateral non-damaged sides of the brain were examined. In the damaged side of the brain, vasogenic edema appeared first, followed by cellular edema. The aggravated cellular edema in the damaged side of the brain resulted in two periods of peak edema severity. Pathological changes in the contralateral non-damaged side of the brain occurred later than those in the damaged side; cellular edema appeared first, followed by vasogenic edema, which was alleviated earlier than the cellular edema. AQP4 was downregulated during vasogenic edema, and upregulated during cellular edema. Taken together, these results suggested that the downregulation of AQP4 was a result of vasogenic edema and that the upregulation of AQP4 may have induced cellular edema. |
format | Online Article Text |
id | pubmed-4626127 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-46261272016-02-23 Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury ZHANG, CHENGCHENG CHEN, JIANQIANG LU, HONG Mol Med Rep Articles Aquaporin 4 (AQP4) is a widely distributed membrane protein, which is found in glial cells, ependymocytes and capillary endothelial cells in the brain, and particularly in the choroid plexus. AQP4 is a key regulator of water metabolism, and changes in its expression following brain injury are associated with pathological changes in the damaged side of the brain; however, the effects of brain injury on AQP4 and injury-induced pathological changes in the contralateral non-damaged side of the brain remain to be fully elucidated. In the present study, male Sprague-Dawley rats were subjected to traumatic brain injury (TBI) and changes in brain water content, the expression of AQP4 expression and pathological characteristics in the damaged and contralateral non-damaged sides of the brain were examined. In the damaged side of the brain, vasogenic edema appeared first, followed by cellular edema. The aggravated cellular edema in the damaged side of the brain resulted in two periods of peak edema severity. Pathological changes in the contralateral non-damaged side of the brain occurred later than those in the damaged side; cellular edema appeared first, followed by vasogenic edema, which was alleviated earlier than the cellular edema. AQP4 was downregulated during vasogenic edema, and upregulated during cellular edema. Taken together, these results suggested that the downregulation of AQP4 was a result of vasogenic edema and that the upregulation of AQP4 may have induced cellular edema. D.A. Spandidos 2015-11 2015-09-25 /pmc/articles/PMC4626127/ /pubmed/26459070 http://dx.doi.org/10.3892/mmr.2015.4372 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles ZHANG, CHENGCHENG CHEN, JIANQIANG LU, HONG Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title | Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title_full | Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title_fullStr | Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title_full_unstemmed | Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title_short | Expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
title_sort | expression of aquaporin-4 and pathological characteristics of brain injury in a rat model of traumatic brain injury |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4626127/ https://www.ncbi.nlm.nih.gov/pubmed/26459070 http://dx.doi.org/10.3892/mmr.2015.4372 |
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