The Role of IL-13 and IL-4 in Adipose Tissue Fibrosis
White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases....
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Published in | International journal of molecular sciences Vol. 24; no. 6; p. 5672 |
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Main Authors | , , , , , , , , , , |
Format | Journal Article |
Language | English |
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Abstract | White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking
, which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas
and
correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated. |
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AbstractList | White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking il4ra, which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas IL13 and IL4 correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated. White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking , which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas and correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated. White adipose tissue (WAT) fibrosis, characterized by an excess of extracellular (ECM) matrix components, is strongly associated with WAT inflammation and dysfunction due to obesity. Interleukin (IL)-13 and IL-4 were recently identified as critical mediators in the pathogenesis of fibrotic diseases. However, their role in WAT fibrosis is still ill-defined. We therefore established an ex vivo WAT organotypic culture system and demonstrated an upregulation of fibrosis-related genes and an increase of α-smooth muscle actin (αSMA) and fibronectin abundance upon dose-dependent stimulation with IL-13/IL-4. These fibrotic effects were lost in WAT lacking il4ra , which encodes for the underlying receptor controlling this process. Adipose tissue macrophages were found to play a key role in mediating IL-13/IL-4 effects in WAT fibrosis as their depletion through clodronate dramatically decreased the fibrotic phenotype. IL-4-induced WAT fibrosis was partly confirmed in mice injected intraperitoneally with IL-4. Furthermore, gene correlation analyses of human WAT samples revealed a strong positive correlation of fibrosis markers with IL-13/IL-4 receptors, whereas IL13 and IL4 correlations failed to confirm this association. In conclusion, IL-13 and IL-4 can induce WAT fibrosis ex vivo and partly in vivo, but their role in human WAT remains to be further elucidated. |
Audience | Academic |
Author | Alexaki, Vasileia-Ismini Hoffmann, Anne Ghosh, Adhideb Wolfrum, Christian Neugebauer, Julia Gericke, Martin Arndt, Lilli Hobusch, Constance Blüher, Matthias Lindhorst, Andreas Glaß, Markus |
AuthorAffiliation | 4 Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Dresden, 01307 Dresden, Germany 2 Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Wittenberg, 06108 Halle (Saale), Germany 1 Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany 7 Institute of Molecular Medicine, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany 5 Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland 3 Helmholtz Institute for Metabolic, Obesity and Vascular Research, 04103 Leipzig, Germany 6 Functional Genomics Center Zurich, ETH Zurich and University of Zurich, 8057 Zurich, Switzerland |
AuthorAffiliation_xml | – name: 1 Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany – name: 3 Helmholtz Institute for Metabolic, Obesity and Vascular Research, 04103 Leipzig, Germany – name: 2 Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Wittenberg, 06108 Halle (Saale), Germany – name: 6 Functional Genomics Center Zurich, ETH Zurich and University of Zurich, 8057 Zurich, Switzerland – name: 4 Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Dresden, 01307 Dresden, Germany – name: 5 Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland – name: 7 Institute of Molecular Medicine, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany |
Author_xml | – sequence: 1 givenname: Lilli orcidid: 0000-0003-2280-1303 surname: Arndt fullname: Arndt, Lilli organization: Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Wittenberg, 06108 Halle (Saale), Germany – sequence: 2 givenname: Andreas surname: Lindhorst fullname: Lindhorst, Andreas organization: Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany – sequence: 3 givenname: Julia orcidid: 0009-0007-1024-8543 surname: Neugebauer fullname: Neugebauer, Julia organization: Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany – sequence: 4 givenname: Anne surname: Hoffmann fullname: Hoffmann, Anne organization: Helmholtz Institute for Metabolic, Obesity and Vascular Research, 04103 Leipzig, Germany – sequence: 5 givenname: Constance surname: Hobusch fullname: Hobusch, Constance organization: Institute of Anatomy, Leipzig University, 04103 Leipzig, Germany – sequence: 6 givenname: Vasileia-Ismini surname: Alexaki fullname: Alexaki, Vasileia-Ismini organization: Institute of Clinical Chemistry and Laboratory Medicine, University Hospital Dresden, 01307 Dresden, Germany – sequence: 7 givenname: Adhideb orcidid: 0000-0002-5160-4571 surname: Ghosh fullname: Ghosh, Adhideb organization: Functional Genomics Center Zurich, ETH Zurich and University of Zurich, 8057 Zurich, Switzerland – sequence: 8 givenname: Matthias orcidid: 0000-0003-0208-2065 surname: Blüher fullname: Blüher, Matthias organization: Helmholtz Institute for Metabolic, Obesity and Vascular Research, 04103 Leipzig, Germany – sequence: 9 givenname: Christian surname: Wolfrum fullname: Wolfrum, Christian organization: Institute of Food, Nutrition and Health, ETH Zurich, 8603 Schwerzenbach, Switzerland – sequence: 10 givenname: Markus orcidid: 0000-0003-2718-8907 surname: Glaß fullname: Glaß, Markus organization: Institute of Molecular Medicine, Martin-Luther-University Halle-Wittenberg, 06120 Halle (Saale), Germany – sequence: 11 givenname: Martin surname: Gericke fullname: Gericke, Martin organization: Institute of Anatomy and Cell Biology, Martin-Luther-University Halle-Wittenberg, 06108 Halle (Saale), Germany |
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SubjectTerms | Actin Adipocytes Adipose tissue Adipose Tissue - pathology Adipose Tissue, White - pathology Adipose tissues Analysis Animals B cells Bisphosphonates Body fat Clodronic acid Collagen Correlation analysis Cytokines Depletion Extracellular matrix Fibroblasts Fibronectin Fibronectins Fibrosis Genetic aspects Genotype & phenotype Humans IL-13 IL-4 Inflammation Interleukin 13 Interleukin 4 Interleukin-13 - genetics Interleukin-4 - genetics Interleukins Lipids Macrophages Metabolism Mice Obesity Pathogenesis Phenotypes Scientific equipment and supplies industry Smooth muscle Type 2 diabetes |
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Title | The Role of IL-13 and IL-4 in Adipose Tissue Fibrosis |
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