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Expression and localization of absent in melanoma 2 in the injured spinal cord
In traumatic brain injury, absent in melanoma 2 (AIM2) has been demonstrated to be involved in pyroptotic neuronal cell death. Although the pathophysiological mechanism of spinal cord injury is similar to that of brain injury, the expression and cellular localization of AIM2 after spinal cord injury...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Medknow Publications & Media Pvt Ltd
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334600/ https://www.ncbi.nlm.nih.gov/pubmed/30539825 http://dx.doi.org/10.4103/1673-5374.245481 |
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author | Wang, Sai-Nan Guo, Xue-Yan Tang, Jie Ding, Shu-Qin Shen, Lin Wang, Rui Ma, Shan-Feng Hu, Jian-Guo Lü, He-Zuo |
author_facet | Wang, Sai-Nan Guo, Xue-Yan Tang, Jie Ding, Shu-Qin Shen, Lin Wang, Rui Ma, Shan-Feng Hu, Jian-Guo Lü, He-Zuo |
author_sort | Wang, Sai-Nan |
collection | PubMed |
description | In traumatic brain injury, absent in melanoma 2 (AIM2) has been demonstrated to be involved in pyroptotic neuronal cell death. Although the pathophysiological mechanism of spinal cord injury is similar to that of brain injury, the expression and cellular localization of AIM2 after spinal cord injury is still not very clear. In the present study, we used a rat model of T9 spinal cord contusive injury, produced using the weight drop method. The rats were randomly divided into 1-hour, 6-hour, 1-day, 3-day and 6-day (post-injury time points) groups. Sham-operated rats only received laminectomy at T9 without contusive injury. Western blot assay revealed that the expression levels of AIM2 were not significantly different among the 1-hour, 6-hour and 1-day groups. The expression levels of AIM2 were markedly higher in the 1-hour, 6-hour and 1-day groups compared with the sham, 3-day and 7-day groups. Double immunofluorescence staining demonstrated that AIM2 was expressed by NeuN(+) (neurons), GFAP(+) (astrocytes), CNPase(+) (oligodendrocytes) and CD11b(+) (microglia) cells in the sham-operated spinal cord. In rats with spinal cord injury, AIM2 was also found in CD45(+) (leukocytes) and CD68(+) (activated microglia/macrophages) cells in the spinal cord at all time points. These findings indicate that AIM2 is mainly expressed in neurons, astrocytes, microglia and oligodendrocytes in the normal spinal cord, and that after spinal cord injury, its expression increases because of the infiltration of leukocytes and the activation of astrocytes and microglia/macrophages. |
format | Online Article Text |
id | pubmed-6334600 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Medknow Publications & Media Pvt Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-63346002019-03-01 Expression and localization of absent in melanoma 2 in the injured spinal cord Wang, Sai-Nan Guo, Xue-Yan Tang, Jie Ding, Shu-Qin Shen, Lin Wang, Rui Ma, Shan-Feng Hu, Jian-Guo Lü, He-Zuo Neural Regen Res Research Article In traumatic brain injury, absent in melanoma 2 (AIM2) has been demonstrated to be involved in pyroptotic neuronal cell death. Although the pathophysiological mechanism of spinal cord injury is similar to that of brain injury, the expression and cellular localization of AIM2 after spinal cord injury is still not very clear. In the present study, we used a rat model of T9 spinal cord contusive injury, produced using the weight drop method. The rats were randomly divided into 1-hour, 6-hour, 1-day, 3-day and 6-day (post-injury time points) groups. Sham-operated rats only received laminectomy at T9 without contusive injury. Western blot assay revealed that the expression levels of AIM2 were not significantly different among the 1-hour, 6-hour and 1-day groups. The expression levels of AIM2 were markedly higher in the 1-hour, 6-hour and 1-day groups compared with the sham, 3-day and 7-day groups. Double immunofluorescence staining demonstrated that AIM2 was expressed by NeuN(+) (neurons), GFAP(+) (astrocytes), CNPase(+) (oligodendrocytes) and CD11b(+) (microglia) cells in the sham-operated spinal cord. In rats with spinal cord injury, AIM2 was also found in CD45(+) (leukocytes) and CD68(+) (activated microglia/macrophages) cells in the spinal cord at all time points. These findings indicate that AIM2 is mainly expressed in neurons, astrocytes, microglia and oligodendrocytes in the normal spinal cord, and that after spinal cord injury, its expression increases because of the infiltration of leukocytes and the activation of astrocytes and microglia/macrophages. Medknow Publications & Media Pvt Ltd 2019-03 /pmc/articles/PMC6334600/ /pubmed/30539825 http://dx.doi.org/10.4103/1673-5374.245481 Text en Copyright: © Neural Regeneration Research http://creativecommons.org/licenses/by-nc-sa/4.0 This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms. |
spellingShingle | Research Article Wang, Sai-Nan Guo, Xue-Yan Tang, Jie Ding, Shu-Qin Shen, Lin Wang, Rui Ma, Shan-Feng Hu, Jian-Guo Lü, He-Zuo Expression and localization of absent in melanoma 2 in the injured spinal cord |
title | Expression and localization of absent in melanoma 2 in the injured spinal cord |
title_full | Expression and localization of absent in melanoma 2 in the injured spinal cord |
title_fullStr | Expression and localization of absent in melanoma 2 in the injured spinal cord |
title_full_unstemmed | Expression and localization of absent in melanoma 2 in the injured spinal cord |
title_short | Expression and localization of absent in melanoma 2 in the injured spinal cord |
title_sort | expression and localization of absent in melanoma 2 in the injured spinal cord |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6334600/ https://www.ncbi.nlm.nih.gov/pubmed/30539825 http://dx.doi.org/10.4103/1673-5374.245481 |
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