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Interferon stimulated gene 15 has an anti-apoptotic effect on MIN6 cells

Atsushi Yoshikawa1, Akihisa Imagawa, Shinsuke Nakata

  • 1Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan.

Endocrine Journal
|July 18, 2014
PubMed

Insights

Interferon stimulated gene (ISG) 15 protects pancreatic beta cells from apoptosis, a key process in type 1 diabetes development. Enhancing ISG15 in beta cells may offer a new therapeutic strategy for type 1 diabetes.

Area of Science:

  • Immunology
  • Endocrinology
  • Molecular Biology

Background:

  • Type 1 diabetes involves pancreatic beta cell destruction, potentially triggered by viral infections.
  • Interferon stimulated gene (ISG) 15 is an antiviral protein whose role in type 1 diabetes pathogenesis is unclear.

Purpose of the Study:

  • To investigate the function of ISG15 in the apoptosis of pancreatic beta cells, a critical factor in type 1 diabetes.

Main Methods:

  • Utilized the MIN6 mouse beta cell line.
  • Stimulated cells with interferon alpha, interleukin-1beta, interferon gamma, and tumor necrosis factor alpha.
  • Assessed apoptosis using caspase 3/7 activity and annexin V assays.
  • Manipulated ISG15 levels using adenovirus-mediated gene expression and short hairpin RNA interference.

Main Results:

  • ISG15 and ISG15-conjugated proteins increased in MIN6 cells upon interferon alpha stimulation.
  • Pretreatment with ISG15 reduced apoptosis in MIN6 cells exposed to inflammatory cytokines.
  • ISG15 knockdown using shRNA increased MIN6 cell apoptosis.

Conclusions:

  • ISG15 exhibits a significant anti-apoptotic effect on pancreatic beta cells.
  • Upregulating ISG15 in pancreatic beta cells presents a potential therapeutic avenue for type 1 diabetes.

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