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Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models

Traumatic spinal cord injury (SCI) is a detrimental condition that causes loss of sensory and motor function in an individual. Many complex secondary injury cascades occur after SCI and they offer great potential for therapeutic targeting. In this study, we investigated the response of endogenous ne...

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Autores principales: Nguyen, Tara, Mao, Yilin, Sutherland, Theresa, Gorrie, Catherine Anne
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5745844/
https://www.ncbi.nlm.nih.gov/pubmed/29239336
http://dx.doi.org/10.4103/1673-5374.219051
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author Nguyen, Tara
Mao, Yilin
Sutherland, Theresa
Gorrie, Catherine Anne
author_facet Nguyen, Tara
Mao, Yilin
Sutherland, Theresa
Gorrie, Catherine Anne
author_sort Nguyen, Tara
collection PubMed
description Traumatic spinal cord injury (SCI) is a detrimental condition that causes loss of sensory and motor function in an individual. Many complex secondary injury cascades occur after SCI and they offer great potential for therapeutic targeting. In this study, we investigated the response of endogenous neural progenitor cells, astrocytes, and microglia to a localized thoracic SCI throughout the neuroaxis. Twenty-five adult female Sprague-Dawley rats underwent mild-contusion thoracic SCI (n = 9), sham surgery (n = 8), or no surgery (n = 8). Spinal cord and brain tissues were fixed and cut at six regions of the neuroaxis. Immunohistochemistry showed increased reactivity of neural progenitor cell marker nestin in the central canal at all levels of the spinal cord. Increased reactivity of astrocyte-specific marker glial fibrillary acidic protein was found only at the lesion epicenter. The number of activated microglia was significantly increased at the lesion site, and activated microglia extended to the lumbar enlargement. Phagocytic microglia and macrophages were significantly increased only at the lesion site. There were no changes in nestin, glial fibrillary acidic protein, microglia and macrophage response in the third ventricle of rats subjected to mild-contusion thoracic SCI compared to the sham surgery or no surgery. These findings indicate that neural progenitor cells, astrocytes and microglia respond differently to a localized SCI, presumably due to differences in inflammatory signaling. These different cellular responses may have implications in the way that neural progenitor cells can be manipulated for neuroregeneration after SCI. This needs to be further investigated.
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spelling pubmed-57458442018-01-02 Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models Nguyen, Tara Mao, Yilin Sutherland, Theresa Gorrie, Catherine Anne Neural Regen Res Research Article Traumatic spinal cord injury (SCI) is a detrimental condition that causes loss of sensory and motor function in an individual. Many complex secondary injury cascades occur after SCI and they offer great potential for therapeutic targeting. In this study, we investigated the response of endogenous neural progenitor cells, astrocytes, and microglia to a localized thoracic SCI throughout the neuroaxis. Twenty-five adult female Sprague-Dawley rats underwent mild-contusion thoracic SCI (n = 9), sham surgery (n = 8), or no surgery (n = 8). Spinal cord and brain tissues were fixed and cut at six regions of the neuroaxis. Immunohistochemistry showed increased reactivity of neural progenitor cell marker nestin in the central canal at all levels of the spinal cord. Increased reactivity of astrocyte-specific marker glial fibrillary acidic protein was found only at the lesion epicenter. The number of activated microglia was significantly increased at the lesion site, and activated microglia extended to the lumbar enlargement. Phagocytic microglia and macrophages were significantly increased only at the lesion site. There were no changes in nestin, glial fibrillary acidic protein, microglia and macrophage response in the third ventricle of rats subjected to mild-contusion thoracic SCI compared to the sham surgery or no surgery. These findings indicate that neural progenitor cells, astrocytes and microglia respond differently to a localized SCI, presumably due to differences in inflammatory signaling. These different cellular responses may have implications in the way that neural progenitor cells can be manipulated for neuroregeneration after SCI. This needs to be further investigated. Medknow Publications & Media Pvt Ltd 2017-11 /pmc/articles/PMC5745844/ /pubmed/29239336 http://dx.doi.org/10.4103/1673-5374.219051 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.
spellingShingle Research Article
Nguyen, Tara
Mao, Yilin
Sutherland, Theresa
Gorrie, Catherine Anne
Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title_full Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title_fullStr Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title_full_unstemmed Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title_short Neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
title_sort neural progenitor cells but not astrocytes respond distally to thoracic spinal cord injury in rat models
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5745844/
https://www.ncbi.nlm.nih.gov/pubmed/29239336
http://dx.doi.org/10.4103/1673-5374.219051
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