Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes

Abstract High serum concentrations of TNF-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor protein family, are found in patients with increased BMI and serum lipid levels. In a model of murine obesity, both the expression of TRAIL and its receptor (TRAIL-R) is elevate...

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Autores principales:	Verena Zoller, Jan-Bernd Funcke, Julian Roos, Meike Dahlhaus, Muad Abd El Hay, Karlheinz Holzmann, Ralf Marienfeld, Thomas Kietzmann, Klaus-Michael Debatin, Martin Wabitsch, Pamela Fischer-Posovszky
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b533c20e2c264adf9a50186b0fc78b9b
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spelling	oai:doaj.org-article:b533c20e2c264adf9a50186b0fc78b9b2021-12-02T12:30:42ZTrail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes10.1038/s41598-017-05932-72045-2322https://doaj.org/article/b533c20e2c264adf9a50186b0fc78b9b2017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-05932-7https://doaj.org/toc/2045-2322Abstract High serum concentrations of TNF-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor protein family, are found in patients with increased BMI and serum lipid levels. In a model of murine obesity, both the expression of TRAIL and its receptor (TRAIL-R) is elevated in adipose tissue. Accordingly, TRAIL has been proposed as an important mediator of adipose tissue inflammation and obesity-associated diseases. The aim of this study was to investigate if TRAIL regulates inflammatory processes at the level of the adipocyte. Using human Simpson-Golabi-Behmel syndrome (SGBS) cells as a model system, we found that TRAIL induces an inflammatory response in both preadipocytes and adipocytes. It stimulates the expression of interleukin 6 (IL-6), interleukin 8 (IL-8) as well as the chemokines monocyte chemoattractant protein-1 (MCP-1) and chemokine C-C motif ligand 20 (CCL-20) in a time- and dose-dependent manner. By using small molecule inhibitors, we found that both the NFκB and the ERK1/2 pathway are crucial for mediating the effect of TRAIL. Taken together, we identified a novel pro-inflammatory function of TRAIL in human adipocytes. Our findings suggest that targeting the TRAIL/TRAIL-R system might be a useful strategy to tackle obesity-associated adipose tissue inflammation.Verena ZollerJan-Bernd FunckeJulian RoosMeike DahlhausMuad Abd El HayKarlheinz HolzmannRalf MarienfeldThomas KietzmannKlaus-Michael DebatinMartin WabitschPamela Fischer-PosovszkyNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-12 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Verena Zoller Jan-Bernd Funcke Julian Roos Meike Dahlhaus Muad Abd El Hay Karlheinz Holzmann Ralf Marienfeld Thomas Kietzmann Klaus-Michael Debatin Martin Wabitsch Pamela Fischer-Posovszky Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
description	Abstract High serum concentrations of TNF-related apoptosis-inducing ligand (TRAIL), a member of the tumor necrosis factor protein family, are found in patients with increased BMI and serum lipid levels. In a model of murine obesity, both the expression of TRAIL and its receptor (TRAIL-R) is elevated in adipose tissue. Accordingly, TRAIL has been proposed as an important mediator of adipose tissue inflammation and obesity-associated diseases. The aim of this study was to investigate if TRAIL regulates inflammatory processes at the level of the adipocyte. Using human Simpson-Golabi-Behmel syndrome (SGBS) cells as a model system, we found that TRAIL induces an inflammatory response in both preadipocytes and adipocytes. It stimulates the expression of interleukin 6 (IL-6), interleukin 8 (IL-8) as well as the chemokines monocyte chemoattractant protein-1 (MCP-1) and chemokine C-C motif ligand 20 (CCL-20) in a time- and dose-dependent manner. By using small molecule inhibitors, we found that both the NFκB and the ERK1/2 pathway are crucial for mediating the effect of TRAIL. Taken together, we identified a novel pro-inflammatory function of TRAIL in human adipocytes. Our findings suggest that targeting the TRAIL/TRAIL-R system might be a useful strategy to tackle obesity-associated adipose tissue inflammation.
format	article
author	Verena Zoller Jan-Bernd Funcke Julian Roos Meike Dahlhaus Muad Abd El Hay Karlheinz Holzmann Ralf Marienfeld Thomas Kietzmann Klaus-Michael Debatin Martin Wabitsch Pamela Fischer-Posovszky
author_facet	Verena Zoller Jan-Bernd Funcke Julian Roos Meike Dahlhaus Muad Abd El Hay Karlheinz Holzmann Ralf Marienfeld Thomas Kietzmann Klaus-Michael Debatin Martin Wabitsch Pamela Fischer-Posovszky
author_sort	Verena Zoller
title	Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
title_short	Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
title_full	Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
title_fullStr	Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
title_full_unstemmed	Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
title_sort	trail (tnf-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b533c20e2c264adf9a50186b0fc78b9b
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Trail (TNF-related apoptosis-inducing ligand) induces an inflammatory response in human adipocytes

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