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MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats
Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activat...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903447/ https://www.ncbi.nlm.nih.gov/pubmed/33732337 http://dx.doi.org/10.3892/etm.2021.9795 |
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author | Ning, Bo Li, Zhen Ning, Lei Wu, Jun Chen, Xin Jiang, Pengjun Lin, Fuxin Zhao, Bing |
author_facet | Ning, Bo Li, Zhen Ning, Lei Wu, Jun Chen, Xin Jiang, Pengjun Lin, Fuxin Zhao, Bing |
author_sort | Ning, Bo |
collection | PubMed |
description | Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activated protein kinase 1 (MSK1) causes the phosphorylation of NF-κB and regulates the activity of pro-inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague-Dawley rats. Hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL-1β and TNF-α in the inflammatory process after SAH. In a model of lipopolysaccharide-induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF-α and IL-1β expression levels, and reached peak levels 2 days after TNF-α and IL-1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF-α and IL-1β in the brain cortex. Furthermore, the in vitro studies indicated that the overexpression of MSK1 inhibited the expression of TNF-α and IL-1β following LPS challenge. These results imply that MSK1 may be involved in the inflammatory reaction following SAH, and may potentially serve as a negative regulator of inflammation. |
format | Online Article Text |
id | pubmed-7903447 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-79034472021-03-16 MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats Ning, Bo Li, Zhen Ning, Lei Wu, Jun Chen, Xin Jiang, Pengjun Lin, Fuxin Zhao, Bing Exp Ther Med Articles Subarachnoid hemorrhage (SAH) is a life-threatening neurological disease. Recently, inflammatory factors have been confirmed to be responsible for the brain damage associated with SAH. Therefore, studying the post-SAH inflammatory reaction may clarify the mechanism of SAH. Mitogen and stress-activated protein kinase 1 (MSK1) causes the phosphorylation of NF-κB and regulates the activity of pro-inflammatory transcription factors. The present study aimed to identify the potential role of MSK1 in inflammation and brain damage development following SAH. A cisterna magna blood injection model was established in Sprague-Dawley rats. Hematoxylin and eosin staining, reverse transcription-quantitative polymerase chain reaction assays and double immunofluorescence staining were used to analyze the role of MSK1, IL-1β and TNF-α in the inflammatory process after SAH. In a model of lipopolysaccharide-induced astrocyte inflammation, the effect of overexpressing MSK1 overexpression was analyzed by western blot analysis. The results demonstrated that MSK1 expression were negatively correlated with TNF-α and IL-1β expression levels, and reached peak levels 2 days after TNF-α and IL-1β. The double immunofluorescence staining results showed that the expression of MSK1 was in the same plane of view as TNF-α and IL-1β in the brain cortex. Furthermore, the in vitro studies indicated that the overexpression of MSK1 inhibited the expression of TNF-α and IL-1β following LPS challenge. These results imply that MSK1 may be involved in the inflammatory reaction following SAH, and may potentially serve as a negative regulator of inflammation. D.A. Spandidos 2021-04 2021-02-18 /pmc/articles/PMC7903447/ /pubmed/33732337 http://dx.doi.org/10.3892/etm.2021.9795 Text en Copyright: © Ning 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 Ning, Bo Li, Zhen Ning, Lei Wu, Jun Chen, Xin Jiang, Pengjun Lin, Fuxin Zhao, Bing MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title | MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title_full | MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title_fullStr | MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title_full_unstemmed | MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title_short | MSK1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
title_sort | msk1 downregulation is involved in inflammatory responses following subarachnoid hemorrhage in rats |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7903447/ https://www.ncbi.nlm.nih.gov/pubmed/33732337 http://dx.doi.org/10.3892/etm.2021.9795 |
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