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Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation
Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. However, the molecular mechanisms limiting macrophage activation are not completely understood. Members of the tripartite motif (TRIM) family have recently emerged as important play...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314404/ https://www.ncbi.nlm.nih.gov/pubmed/28211536 http://dx.doi.org/10.1038/srep42781 |
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author | Jiang, Mei-Xiu Hong, Xuan Liao, Bin-Bin Shi, Shui-Zhen Lai, Xiao-Fang Zheng, Huai-Yu Xie, Lin Wang, Yuan Wang, Xiao-Lei Xin, Hong-Bo Fu, Mingui Deng, Ke-Yu |
author_facet | Jiang, Mei-Xiu Hong, Xuan Liao, Bin-Bin Shi, Shui-Zhen Lai, Xiao-Fang Zheng, Huai-Yu Xie, Lin Wang, Yuan Wang, Xiao-Lei Xin, Hong-Bo Fu, Mingui Deng, Ke-Yu |
author_sort | Jiang, Mei-Xiu |
collection | PubMed |
description | Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. However, the molecular mechanisms limiting macrophage activation are not completely understood. Members of the tripartite motif (TRIM) family have recently emerged as important players in innate immunity and antivirus. Here, we systematically analyzed mRNA expressions of representative TRIM molecules in human THP1-derived macrophages activated by different toll-like receptor (TLR) ligands. Twenty-nine TRIM members were highly induced (>3 fold) by one or more TLR ligands, among which 19 of them belong to TRIM C-IV subgroup. Besides TRIM21, TRIM22 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identified a novel group of TRIM genes (TRIM14, 15, 31, 34, 43, 48, 49, 51 and 61) that were significantly up-regulated by TLR3 and TLR4 ligands. In contrast, the expression of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophages. The alternations of the TRIM proteins were confirmed by Western blot. Finally, overexpression of TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediated knockdown of TRIM59 enhanced LPS-induced macrophage activation. Taken together, the study provided an insight into the TLR ligands-induced expressions of TRIM family in macrophages. |
format | Online Article Text |
id | pubmed-5314404 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-53144042017-02-24 Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation Jiang, Mei-Xiu Hong, Xuan Liao, Bin-Bin Shi, Shui-Zhen Lai, Xiao-Fang Zheng, Huai-Yu Xie, Lin Wang, Yuan Wang, Xiao-Lei Xin, Hong-Bo Fu, Mingui Deng, Ke-Yu Sci Rep Article Activated macrophages play an important role in many inflammatory diseases including septic shock and atherosclerosis. However, the molecular mechanisms limiting macrophage activation are not completely understood. Members of the tripartite motif (TRIM) family have recently emerged as important players in innate immunity and antivirus. Here, we systematically analyzed mRNA expressions of representative TRIM molecules in human THP1-derived macrophages activated by different toll-like receptor (TLR) ligands. Twenty-nine TRIM members were highly induced (>3 fold) by one or more TLR ligands, among which 19 of them belong to TRIM C-IV subgroup. Besides TRIM21, TRIM22 and TRIM38 were shown to be upregulated by TLR3 and TLR4 ligands as previous reported, we identified a novel group of TRIM genes (TRIM14, 15, 31, 34, 43, 48, 49, 51 and 61) that were significantly up-regulated by TLR3 and TLR4 ligands. In contrast, the expression of TRIM59 was down-regulated by TLR3 and TLR4 ligands in both human and mouse macrophages. The alternations of the TRIM proteins were confirmed by Western blot. Finally, overexpression of TRIM59 significantly suppressed LPS-induced macrophage activation, whereas siRNA-mediated knockdown of TRIM59 enhanced LPS-induced macrophage activation. Taken together, the study provided an insight into the TLR ligands-induced expressions of TRIM family in macrophages. Nature Publishing Group 2017-02-17 /pmc/articles/PMC5314404/ /pubmed/28211536 http://dx.doi.org/10.1038/srep42781 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Jiang, Mei-Xiu Hong, Xuan Liao, Bin-Bin Shi, Shui-Zhen Lai, Xiao-Fang Zheng, Huai-Yu Xie, Lin Wang, Yuan Wang, Xiao-Lei Xin, Hong-Bo Fu, Mingui Deng, Ke-Yu Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title | Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title_full | Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title_fullStr | Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title_full_unstemmed | Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title_short | Expression profiling of TRIM protein family in THP1-derived macrophages following TLR stimulation |
title_sort | expression profiling of trim protein family in thp1-derived macrophages following tlr stimulation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5314404/ https://www.ncbi.nlm.nih.gov/pubmed/28211536 http://dx.doi.org/10.1038/srep42781 |
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