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Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage
Microglia-mediated neuroinflammatory response in the early brain injury after subarachnoid hemorrhage (SAH) has been reported to have an impact on progress, and the mechanism is not completely understood. Here, we performed genome-wide transcriptome analysis of microglia purified from damaged hemisp...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278202/ https://www.ncbi.nlm.nih.gov/pubmed/34276335 http://dx.doi.org/10.3389/fnagi.2021.645649 |
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author | Xu, Shenbin Mei, Shuhao Lu, Jianan Wu, Haijian Dong, Xiao Shi, Ligen Zhou, Jingyi Zhang, Jianmin |
author_facet | Xu, Shenbin Mei, Shuhao Lu, Jianan Wu, Haijian Dong, Xiao Shi, Ligen Zhou, Jingyi Zhang, Jianmin |
author_sort | Xu, Shenbin |
collection | PubMed |
description | Microglia-mediated neuroinflammatory response in the early brain injury after subarachnoid hemorrhage (SAH) has been reported to have an impact on progress, and the mechanism is not completely understood. Here, we performed genome-wide transcriptome analysis of microglia purified from damaged hemisphere of adult mice at 3 days after SAH or sham operation. Robust transcriptional changes were observed between SAH-induced and healthy microglia, indicating rapid activation of microglia after suffering from SAH. We identified 1576 differentially expressed genes (DEGs; 928 upregulated and 648 downregulated) in SAH-induced microglia compared with sham microglia, representing a strong alteration of the genome (6.85% of total ∼23,000 genes). Functional enrichment of these DEGs indicated that cell division, inflammatory response, cytokine production, and leukocyte chemotaxis were strongly activated in SAH-induced microglia. Moreover, we identified and proved that the TLR2/IRF7 signaling axis was involved in the regulation of this microglia-mediated inflammation in SAH mice by performing flow cytometry and immunofluorescence. Together, these results provided a perspective of microglia-mediated neuroinflammatory response in the early stage of SAH and might give a new therapeutic target for SAH. |
format | Online Article Text |
id | pubmed-8278202 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82782022021-07-15 Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage Xu, Shenbin Mei, Shuhao Lu, Jianan Wu, Haijian Dong, Xiao Shi, Ligen Zhou, Jingyi Zhang, Jianmin Front Aging Neurosci Neuroscience Microglia-mediated neuroinflammatory response in the early brain injury after subarachnoid hemorrhage (SAH) has been reported to have an impact on progress, and the mechanism is not completely understood. Here, we performed genome-wide transcriptome analysis of microglia purified from damaged hemisphere of adult mice at 3 days after SAH or sham operation. Robust transcriptional changes were observed between SAH-induced and healthy microglia, indicating rapid activation of microglia after suffering from SAH. We identified 1576 differentially expressed genes (DEGs; 928 upregulated and 648 downregulated) in SAH-induced microglia compared with sham microglia, representing a strong alteration of the genome (6.85% of total ∼23,000 genes). Functional enrichment of these DEGs indicated that cell division, inflammatory response, cytokine production, and leukocyte chemotaxis were strongly activated in SAH-induced microglia. Moreover, we identified and proved that the TLR2/IRF7 signaling axis was involved in the regulation of this microglia-mediated inflammation in SAH mice by performing flow cytometry and immunofluorescence. Together, these results provided a perspective of microglia-mediated neuroinflammatory response in the early stage of SAH and might give a new therapeutic target for SAH. Frontiers Media S.A. 2021-06-30 /pmc/articles/PMC8278202/ /pubmed/34276335 http://dx.doi.org/10.3389/fnagi.2021.645649 Text en Copyright © 2021 Xu, Mei, Lu, Wu, Dong, Shi, Zhou and Zhang. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Xu, Shenbin Mei, Shuhao Lu, Jianan Wu, Haijian Dong, Xiao Shi, Ligen Zhou, Jingyi Zhang, Jianmin Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title | Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title_full | Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title_fullStr | Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title_full_unstemmed | Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title_short | Transcriptome Analysis of Microglia Reveals That the TLR2/IRF7 Signaling Axis Mediates Neuroinflammation After Subarachnoid Hemorrhage |
title_sort | transcriptome analysis of microglia reveals that the tlr2/irf7 signaling axis mediates neuroinflammation after subarachnoid hemorrhage |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8278202/ https://www.ncbi.nlm.nih.gov/pubmed/34276335 http://dx.doi.org/10.3389/fnagi.2021.645649 |
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