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The Complement Inhibitor CD59 Regulates Insulin Secretion by Modulating Exocytotic Events.

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Author

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Summary, in English

Type 2 diabetes is triggered by reduced insulin production, caused by genetic and environmental factors such as inflammation originating from the innate immune system. Complement proteins are a component of innate immunity and kill non-self cells by perforating the plasma membrane, a reaction prevented by CD59. Human pancreatic islets express CD59 at very high levels. CD59 is primarily known as a plasma membrane protein in membrane rafts, but most CD59 protein in pancreatic β cells is intracellular. Removing extracellular CD59 disrupts membrane rafts and moderately stimulates insulin secretion, whereas silencing intracellular CD59 markedly suppresses regulated secretion by exocytosis, as demonstrated by TIRF imaging. CD59 interacts with the exocytotic proteins VAMP2 and Syntaxin-1. CD59 expression is reduced by glucose and in rodent diabetes models but upregulated in human diabetic islets, potentially reflecting compensatory reactions. This unconventional action of CD59 broadens the established view of innate immunity in type 2 diabetes.

Publishing year

2014

Language

English

Pages

883-890

Publication/Series

Cell Metabolism

Volume

19

Issue

5

Document type

Journal article

Publisher

Cell Press

Topic

  • Cell and Molecular Biology

Status

Published

Research group

  • Diabetes - Islet Patophysiology
  • Protein Chemistry, Malmö
  • Diabetic Complications
  • Genomics, Diabetes and Endocrinology
  • Celiac Disease and Diabetes Unit
  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 1550-4131