Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells

Human peritoneal mesothelial cells (MC) play an important role in inflammatory processes of the peritoneal cavity by producing various cytokines and chemokines, such as monocyte chemoattractant protein-1 (MCP-1). The present study was designed to assess the effect of the peroxisome proliferator-acti...

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Main Authors: Matthias Sauter, Kathrin Kastenmüller, Franziska Belling, Markus Wörnle, Roland Ladurner, Thomas Mussack, Thomas Sitter
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Mediators of Inflammation
Online Access:http://dx.doi.org/10.1155/2012/217696
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author Matthias Sauter
Kathrin Kastenmüller
Franziska Belling
Markus Wörnle
Roland Ladurner
Thomas Mussack
Thomas Sitter
author_facet Matthias Sauter
Kathrin Kastenmüller
Franziska Belling
Markus Wörnle
Roland Ladurner
Thomas Mussack
Thomas Sitter
author_sort Matthias Sauter
collection DOAJ
description Human peritoneal mesothelial cells (MC) play an important role in inflammatory processes of the peritoneal cavity by producing various cytokines and chemokines, such as monocyte chemoattractant protein-1 (MCP-1). The present study was designed to assess the effect of the peroxisome proliferator-activated receptor-gamma- (PPARγ-) activator rosiglitazone on the mesothelial MCP-1 expression and release. Primary cultures of MC were obtained from omental tissue. MCP-1 antigen concentrations were measured in the cell supernatant by ELISA and MCP-1 mRNA levels by real-time polymerase chain reaction. The presence of PPARγ on MC was assayed in a Western Blot analysis. MC constitutively express PPARγ. Activation of this receptor via rosiglitazone (0,1–10 μmol/L) resulted in significantly reduced amounts of mesothelial MCP-1 release as well as MCP-1 mRNA. The use of the PPARγ inhibitor GW-9662 could completely prevent the rosiglitazone effects. Rosiglitazone was also effective in reducing TNFα-induced enhanced secretion of MCP-1. Our findings indicate that glitazones are effective in reducing constitutive and TNFα-stimulated mesothelial MCP-1 mRNA expression and release.
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spelling doaj-art-86f47409dcf2400c87b3a8535546429d2025-08-20T03:37:57ZengWileyMediators of Inflammation0962-93511466-18612012-01-01201210.1155/2012/217696217696Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial CellsMatthias Sauter0Kathrin Kastenmüller1Franziska Belling2Markus Wörnle3Roland Ladurner4Thomas Mussack5Thomas Sitter6Medizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Pettenkoferstr. 8a, 80336 Muenchen, GermanyMedizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Pettenkoferstr. 8a, 80336 Muenchen, GermanyMedizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Pettenkoferstr. 8a, 80336 Muenchen, GermanyMedizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Pettenkoferstr. 8a, 80336 Muenchen, GermanyChirurgische Klinik-Innenstadt, Klinikum der Universitaet Muenchen, Nußbaumstr. 20, 80336 Muenchen, GermanyChirurgische Klinik-Innenstadt, Klinikum der Universitaet Muenchen, Nußbaumstr. 20, 80336 Muenchen, GermanyMedizinische Poliklinik-Innenstadt, Klinikum der Universitaet Muenchen, Pettenkoferstr. 8a, 80336 Muenchen, GermanyHuman peritoneal mesothelial cells (MC) play an important role in inflammatory processes of the peritoneal cavity by producing various cytokines and chemokines, such as monocyte chemoattractant protein-1 (MCP-1). The present study was designed to assess the effect of the peroxisome proliferator-activated receptor-gamma- (PPARγ-) activator rosiglitazone on the mesothelial MCP-1 expression and release. Primary cultures of MC were obtained from omental tissue. MCP-1 antigen concentrations were measured in the cell supernatant by ELISA and MCP-1 mRNA levels by real-time polymerase chain reaction. The presence of PPARγ on MC was assayed in a Western Blot analysis. MC constitutively express PPARγ. Activation of this receptor via rosiglitazone (0,1–10 μmol/L) resulted in significantly reduced amounts of mesothelial MCP-1 release as well as MCP-1 mRNA. The use of the PPARγ inhibitor GW-9662 could completely prevent the rosiglitazone effects. Rosiglitazone was also effective in reducing TNFα-induced enhanced secretion of MCP-1. Our findings indicate that glitazones are effective in reducing constitutive and TNFα-stimulated mesothelial MCP-1 mRNA expression and release.http://dx.doi.org/10.1155/2012/217696
spellingShingle Matthias Sauter
Kathrin Kastenmüller
Franziska Belling
Markus Wörnle
Roland Ladurner
Thomas Mussack
Thomas Sitter
Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
Mediators of Inflammation
title Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
title_full Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
title_fullStr Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
title_full_unstemmed Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
title_short Activation of Peroxisome Proliferator-Activated Receptor-Gamma by Glitazones Reduces the Expression and Release of Monocyte Chemoattractant Protein-1 in Human Mesothelial Cells
title_sort activation of peroxisome proliferator activated receptor gamma by glitazones reduces the expression and release of monocyte chemoattractant protein 1 in human mesothelial cells
url http://dx.doi.org/10.1155/2012/217696
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