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Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose
Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix–loop–helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435501/ https://www.ncbi.nlm.nih.gov/pubmed/30420491 http://dx.doi.org/10.1042/BSR20180767 |
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author | Chen, Yan Wang, Yan-Jun Zhao, Ying Wang, Jin-Cheng |
author_facet | Chen, Yan Wang, Yan-Jun Zhao, Ying Wang, Jin-Cheng |
author_sort | Chen, Yan |
collection | PubMed |
description | Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix–loop–helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated the role of ChREBP in the pathogenesis of DN. The expression of ChREBP was detected in patients with type 2 diabetes mellitus (T2DM), diabetic mice, and mesangial cells. ELISA was used to measure cytokine production in mesangial cells. Flow cytometry analysis was performed to detect the apoptosis of mesangial cells in the presence of high glucose. The expression levels of ChREBP and several cytokines (TNF-α, IL-1β, and IL-6) were up-regulated in T2DM patients. The mRNA and protein levels of ChREBP were also significantly elevated in the kidneys of diabetic mice. Moreover, glucose treatment promoted mRNA levels of TNF-α, IL-1β, and IL-6 in mesangial cells. Glucose stimulation induced significant apoptosis of SV40 MES 13 cells. In addition, transfection with ChREBP siRNA significantly inhibited ChREBP expression. Consequently, the inflammatory responses and apoptosis were inhibited in SV40 MES 13 cells. These results demonstrated that ChREBP could mediate the inflammatory response and apoptosis of mesangial cells, suggesting that ChREBP may be involved in the pathogenesis of DN. |
format | Online Article Text |
id | pubmed-6435501 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-64355012019-04-12 Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose Chen, Yan Wang, Yan-Jun Zhao, Ying Wang, Jin-Cheng Biosci Rep Research Articles Diabetic nephropathy (DN) is one of the most devastating complications of diabetes mellitus. Carbohydrate response element binding protein (ChREBP) is a basic helix–loop–helix leucine zipper transcription factor that primarily mediates glucose homeostasis in the body. The present study investigated the role of ChREBP in the pathogenesis of DN. The expression of ChREBP was detected in patients with type 2 diabetes mellitus (T2DM), diabetic mice, and mesangial cells. ELISA was used to measure cytokine production in mesangial cells. Flow cytometry analysis was performed to detect the apoptosis of mesangial cells in the presence of high glucose. The expression levels of ChREBP and several cytokines (TNF-α, IL-1β, and IL-6) were up-regulated in T2DM patients. The mRNA and protein levels of ChREBP were also significantly elevated in the kidneys of diabetic mice. Moreover, glucose treatment promoted mRNA levels of TNF-α, IL-1β, and IL-6 in mesangial cells. Glucose stimulation induced significant apoptosis of SV40 MES 13 cells. In addition, transfection with ChREBP siRNA significantly inhibited ChREBP expression. Consequently, the inflammatory responses and apoptosis were inhibited in SV40 MES 13 cells. These results demonstrated that ChREBP could mediate the inflammatory response and apoptosis of mesangial cells, suggesting that ChREBP may be involved in the pathogenesis of DN. Portland Press Ltd. 2018-12-07 /pmc/articles/PMC6435501/ /pubmed/30420491 http://dx.doi.org/10.1042/BSR20180767 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Research Articles Chen, Yan Wang, Yan-Jun Zhao, Ying Wang, Jin-Cheng Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title | Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title_full | Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title_fullStr | Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title_full_unstemmed | Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title_short | Carbohydrate response element binding protein (ChREBP) modulates the inflammatory response of mesangial cells in response to glucose |
title_sort | carbohydrate response element binding protein (chrebp) modulates the inflammatory response of mesangial cells in response to glucose |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6435501/ https://www.ncbi.nlm.nih.gov/pubmed/30420491 http://dx.doi.org/10.1042/BSR20180767 |
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