il-13 improves beta-cell survival and protects against il-1beta-induced beta-cell death

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ID: 195024
2016
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Abstract
Objectives: IL-13 is a cytokine classically produced by anti-inflammatory T-helper-2 lymphocytes; it is decreased in the circulation of type 2 diabetic patients and impacts positively on liver and skeletal muscle. Although IL-13 can exert positive effects on beta-cell lines, its impact and mode of action on primary beta-cell function and survival remain largely unexplored. Methods: Beta-cells were cultured for 48 h in the presence of IL-13 alone or in combination with IL-1β or cytokine cocktail (IL-1β, IFNγ, TNFα). Results: IL-13 protected human and rat beta-cells against cytokine induced death. However, IL-13 was unable to protect from IL-1β impaired glucose stimulated insulin secretion and did not influence NFκB nuclear relocalization induced by IL-1β. IL-13 induced phosphorylation of Akt, increased IRS2 protein expression and counteracted the IL-1β induced regulation of several beta-cell stress response genes. Conclusions: The prosurvival effects of IL-13 thus appear to be mediated through IRS2/Akt signaling with NFκB independent regulation of gene expression. In addition to previously documented beneficial effects on insulin target tissues, these data suggest that IL-13 may be useful for treatment of type 2 diabetes by preserving beta-cell mass or slowing its rate of decline. Keywords: Beta-cells, Apoptosis, Cytokines, Gene expression, Akt
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rtti2016molecularil-13 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Sabine Rütti, Cédric Howald, Caroline Arous, Emmanouil Dermitzakis, Philippe A. Halban, Karim Bouzakri
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Journal Small (Weinheim an der Bergstrasse, Germany)
Year 2016
DOI
DOI not found
URL
http://www.sciencedirect.com/science/article/pii/S221287781500215X
Keywords
internal medicine

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