Cargando…
Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor
The present study was designed to determine whether sulfur dioxide (SO(2)) could be endogenously produced in adipocyte and served as a novel adipocyte-derived inflammatory inhibitor. SO(2) was detected in adipose tissue using high-performance liquid chromatography with fluorescence detection. SO(2)...
Autores principales: | , , , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887903/ https://www.ncbi.nlm.nih.gov/pubmed/27246393 http://dx.doi.org/10.1038/srep27026 |
_version_ | 1782434794829774848 |
---|---|
author | Zhang, Heng Huang, Yaqian Bu, Dingfang Chen, Selena Tang, Chaoshu Wang, Guang Du, Junbao Jin, Hongfang |
author_facet | Zhang, Heng Huang, Yaqian Bu, Dingfang Chen, Selena Tang, Chaoshu Wang, Guang Du, Junbao Jin, Hongfang |
author_sort | Zhang, Heng |
collection | PubMed |
description | The present study was designed to determine whether sulfur dioxide (SO(2)) could be endogenously produced in adipocyte and served as a novel adipocyte-derived inflammatory inhibitor. SO(2) was detected in adipose tissue using high-performance liquid chromatography with fluorescence detection. SO(2) synthase aspartate aminotransferase (AAT1 and AAT2) mRNA and protein expressions in adipose tissues were measured. For in vitro study, 3T3-L1 adipocytes were cultured, infected with adenovirus carrying AAT1 gene or lentivirus carrying shRNA to AAT1, and then treated with tumor necrosis factor-α (TNF-α). We found that endogenous SO(2)/AAT pathway existed in adipose tissues including perivascular, perirenal, epididymal, subcutaneous and brown adipose tissue. AAT1 overexpression significantly increased SO(2) production and inhibited TNF-α-induced inflammatory factors, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 adipocytes. By contrast, AAT1 knockdown decreased SO(2) production and exacerbated TNF-α-stimulated MCP-1 and IL-8 secretion. Mechanistically, AAT1 overexpression attenuated TNF-α-induced IκBα phosphorylation and degradation, and nuclear factor-κB (NF-κB) p65 phosphorylation, while AAT1 knockdown aggravated TNF-α-activated NF-κB pathway, which was blocked by SO(2). NF-κB inhibitors, PDTC or Bay 11-7082, abolished excessive p65 phosphorylation and adipocyte inflammation induced by AAT1 knockdown. This is the first report to suggest that endogenous SO(2) is a novel adipocyte-derived inflammatory inhibitor. |
format | Online Article Text |
id | pubmed-4887903 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-48879032016-06-09 Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor Zhang, Heng Huang, Yaqian Bu, Dingfang Chen, Selena Tang, Chaoshu Wang, Guang Du, Junbao Jin, Hongfang Sci Rep Article The present study was designed to determine whether sulfur dioxide (SO(2)) could be endogenously produced in adipocyte and served as a novel adipocyte-derived inflammatory inhibitor. SO(2) was detected in adipose tissue using high-performance liquid chromatography with fluorescence detection. SO(2) synthase aspartate aminotransferase (AAT1 and AAT2) mRNA and protein expressions in adipose tissues were measured. For in vitro study, 3T3-L1 adipocytes were cultured, infected with adenovirus carrying AAT1 gene or lentivirus carrying shRNA to AAT1, and then treated with tumor necrosis factor-α (TNF-α). We found that endogenous SO(2)/AAT pathway existed in adipose tissues including perivascular, perirenal, epididymal, subcutaneous and brown adipose tissue. AAT1 overexpression significantly increased SO(2) production and inhibited TNF-α-induced inflammatory factors, monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) secretion from 3T3-L1 adipocytes. By contrast, AAT1 knockdown decreased SO(2) production and exacerbated TNF-α-stimulated MCP-1 and IL-8 secretion. Mechanistically, AAT1 overexpression attenuated TNF-α-induced IκBα phosphorylation and degradation, and nuclear factor-κB (NF-κB) p65 phosphorylation, while AAT1 knockdown aggravated TNF-α-activated NF-κB pathway, which was blocked by SO(2). NF-κB inhibitors, PDTC or Bay 11-7082, abolished excessive p65 phosphorylation and adipocyte inflammation induced by AAT1 knockdown. This is the first report to suggest that endogenous SO(2) is a novel adipocyte-derived inflammatory inhibitor. Nature Publishing Group 2016-06-01 /pmc/articles/PMC4887903/ /pubmed/27246393 http://dx.doi.org/10.1038/srep27026 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 Zhang, Heng Huang, Yaqian Bu, Dingfang Chen, Selena Tang, Chaoshu Wang, Guang Du, Junbao Jin, Hongfang Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title | Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title_full | Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title_fullStr | Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title_full_unstemmed | Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title_short | Endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
title_sort | endogenous sulfur dioxide is a novel adipocyte-derived inflammatory inhibitor |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4887903/ https://www.ncbi.nlm.nih.gov/pubmed/27246393 http://dx.doi.org/10.1038/srep27026 |
work_keys_str_mv | AT zhangheng endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT huangyaqian endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT budingfang endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT chenselena endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT tangchaoshu endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT wangguang endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT dujunbao endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor AT jinhongfang endogenoussulfurdioxideisanoveladipocytederivedinflammatoryinhibitor |