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Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis
New diagnostic biomarkers or therapeutic targets for sepsis have substantial significance for critical care medicine. In this study, 192 differentially expressed proteins were selected through iTRAQ. Based on cluster analysis of protein expression dynamics and protein-protein interactions, hemopexin...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6451033/ https://www.ncbi.nlm.nih.gov/pubmed/30952998 http://dx.doi.org/10.1038/s41598-019-42287-7 |
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author | Su, Longxiang Pan, Pan Yan, Peng Long, Yun Zhou, Xiang Wang, Xiaoting Zhou, Ruo Wen, Bo Xie, Lixin Liu, Dawei |
author_facet | Su, Longxiang Pan, Pan Yan, Peng Long, Yun Zhou, Xiang Wang, Xiaoting Zhou, Ruo Wen, Bo Xie, Lixin Liu, Dawei |
author_sort | Su, Longxiang |
collection | PubMed |
description | New diagnostic biomarkers or therapeutic targets for sepsis have substantial significance for critical care medicine. In this study, 192 differentially expressed proteins were selected through iTRAQ. Based on cluster analysis of protein expression dynamics and protein-protein interactions, hemopexin, vimentin, and heat shock protein 90 were selected for further investigation. It was demonstrated that serum vimentin (VIM) levels were significantly increased in patients with sepsis and septic shock compared to controls and that VIM expression was significantly increased in lymphocytes isolated from septic shock and sepsis patients compared to controls. Moreover, a nonsurvivor group had higher serum VIM levels and VIM expression in lymphocytes. Caspase-3 was significantly upregulated in Jurkat T cells lacking VIM and when exposed to LPS compared to control cells. In contrast, caspase-3 was reduced nearly 40% in cells over-expressing VIM. IL-2, IL-10 and IFN-α levels were significantly decreased in cells lacking VIM compared to control cells, whereas they were not significantly altered in cells over-expressing VIM. These findings suggest that VIM modulates lymphocyte apoptosis and inflammatory responses and that VIM could be a new target for the diagnosis and prognostic prediction of patients with sepsis or septic shock. |
format | Online Article Text |
id | pubmed-6451033 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-64510332019-04-11 Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis Su, Longxiang Pan, Pan Yan, Peng Long, Yun Zhou, Xiang Wang, Xiaoting Zhou, Ruo Wen, Bo Xie, Lixin Liu, Dawei Sci Rep Article New diagnostic biomarkers or therapeutic targets for sepsis have substantial significance for critical care medicine. In this study, 192 differentially expressed proteins were selected through iTRAQ. Based on cluster analysis of protein expression dynamics and protein-protein interactions, hemopexin, vimentin, and heat shock protein 90 were selected for further investigation. It was demonstrated that serum vimentin (VIM) levels were significantly increased in patients with sepsis and septic shock compared to controls and that VIM expression was significantly increased in lymphocytes isolated from septic shock and sepsis patients compared to controls. Moreover, a nonsurvivor group had higher serum VIM levels and VIM expression in lymphocytes. Caspase-3 was significantly upregulated in Jurkat T cells lacking VIM and when exposed to LPS compared to control cells. In contrast, caspase-3 was reduced nearly 40% in cells over-expressing VIM. IL-2, IL-10 and IFN-α levels were significantly decreased in cells lacking VIM compared to control cells, whereas they were not significantly altered in cells over-expressing VIM. These findings suggest that VIM modulates lymphocyte apoptosis and inflammatory responses and that VIM could be a new target for the diagnosis and prognostic prediction of patients with sepsis or septic shock. Nature Publishing Group UK 2019-04-05 /pmc/articles/PMC6451033/ /pubmed/30952998 http://dx.doi.org/10.1038/s41598-019-42287-7 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Su, Longxiang Pan, Pan Yan, Peng Long, Yun Zhou, Xiang Wang, Xiaoting Zhou, Ruo Wen, Bo Xie, Lixin Liu, Dawei Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title | Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title_full | Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title_fullStr | Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title_full_unstemmed | Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title_short | Role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
title_sort | role of vimentin in modulating immune cell apoptosis and inflammatory responses in sepsis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6451033/ https://www.ncbi.nlm.nih.gov/pubmed/30952998 http://dx.doi.org/10.1038/s41598-019-42287-7 |
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