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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...

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Detalles Bibliográficos
Autores principales: Chen, Yan, Wang, Yan-Jun, Zhao, Ying, Wang, Jin-Cheng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
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.
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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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