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Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis
In response to changes in microenvironment, macrophages polarize into functionally distinct phenotypes, playing a crucial role in the pathogenesis of inflammatory bowel disease (IBD). Here, we investigated the effects of sorting nexin 10 (SNX10), a protein involved in endosomal trafficking and osteo...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746623/ https://www.ncbi.nlm.nih.gov/pubmed/26856241 http://dx.doi.org/10.1038/srep20630 |
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author | You, Yan Zhou, Chun Li, Dong Cao, Zhong-Lian Shen, Weixing Li, Wan-Zhen Zhang, Sulin Hu, Bin Shen, Xiaoyan |
author_facet | You, Yan Zhou, Chun Li, Dong Cao, Zhong-Lian Shen, Weixing Li, Wan-Zhen Zhang, Sulin Hu, Bin Shen, Xiaoyan |
author_sort | You, Yan |
collection | PubMed |
description | In response to changes in microenvironment, macrophages polarize into functionally distinct phenotypes, playing a crucial role in the pathogenesis of inflammatory bowel disease (IBD). Here, we investigated the effects of sorting nexin 10 (SNX10), a protein involved in endosomal trafficking and osteoclast maturation, on regulation of macrophage polarization and progression of mouse colitis. Our results revealed that SNX10 deficiency increased the population of M2-type monocytes/macrophages, and protected against colonic inflammation and pathological damage induced by dextran sulfate sodium (DSS). By in vitro study, we showed that deficiency of SNX10 polarized macrophages derived from mouse bone marrow or human peripheral blood mononuclear cells (PBMCs) towards an anti-inflammatory M2 phenotype, which partially reversed by SNX10 plasmid transfection. Adoptive transfer of SNX10(−/−) macrophages ameliorated colitis in WT mice. However, transfer of WT macrophages exacerbated colitis in SNX10(−/−) mice. Our data disclose a crucial role and novel function for SNX10 in macrophage polarization. Loss of SNX10 function may be a potential promising therapeutic strategy for IBD. |
format | Online Article Text |
id | pubmed-4746623 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-47466232016-02-17 Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis You, Yan Zhou, Chun Li, Dong Cao, Zhong-Lian Shen, Weixing Li, Wan-Zhen Zhang, Sulin Hu, Bin Shen, Xiaoyan Sci Rep Article In response to changes in microenvironment, macrophages polarize into functionally distinct phenotypes, playing a crucial role in the pathogenesis of inflammatory bowel disease (IBD). Here, we investigated the effects of sorting nexin 10 (SNX10), a protein involved in endosomal trafficking and osteoclast maturation, on regulation of macrophage polarization and progression of mouse colitis. Our results revealed that SNX10 deficiency increased the population of M2-type monocytes/macrophages, and protected against colonic inflammation and pathological damage induced by dextran sulfate sodium (DSS). By in vitro study, we showed that deficiency of SNX10 polarized macrophages derived from mouse bone marrow or human peripheral blood mononuclear cells (PBMCs) towards an anti-inflammatory M2 phenotype, which partially reversed by SNX10 plasmid transfection. Adoptive transfer of SNX10(−/−) macrophages ameliorated colitis in WT mice. However, transfer of WT macrophages exacerbated colitis in SNX10(−/−) mice. Our data disclose a crucial role and novel function for SNX10 in macrophage polarization. Loss of SNX10 function may be a potential promising therapeutic strategy for IBD. Nature Publishing Group 2016-02-09 /pmc/articles/PMC4746623/ /pubmed/26856241 http://dx.doi.org/10.1038/srep20630 Text en Copyright © 2016, Macmillan Publishers Limited 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 You, Yan Zhou, Chun Li, Dong Cao, Zhong-Lian Shen, Weixing Li, Wan-Zhen Zhang, Sulin Hu, Bin Shen, Xiaoyan Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title | Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title_full | Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title_fullStr | Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title_full_unstemmed | Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title_short | Sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
title_sort | sorting nexin 10 acting as a novel regulator of macrophage polarization mediates inflammatory response in experimental mouse colitis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4746623/ https://www.ncbi.nlm.nih.gov/pubmed/26856241 http://dx.doi.org/10.1038/srep20630 |
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