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

  • Yoshikawa Atsushi
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Imagawa Akihisa
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Nakata Shinsuke
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Fukui Kenji
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Kuroda Yohei
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Miyata Yugo
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Sato Yoshifumi
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Hanafusa Toshiaki
    Department of Internal Medicine (I), Osaka Medical College, Takatsuki 569-8686, Japan
  • Matsuoka Taka-aki
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Kaneto Hideaki
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Iwahashi Hiromi
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan
  • Shimomura Iichiro
    Department of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan

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Description

Type 1 diabetes, one of two major forms of diabetes, results from the complete destruction of pancreatic beta cells. Viral infection has been suggested to be a trigger of beta cell destruction, the pathogenesis of type 1 diabetes. The aim of this study was to clarify the role of the protein encoded by intherferon stimulated gene (ISG) 15, an antiviral effector, in the development of this clinical entity. We used the mouse beta cell line MIN6 to investigate the role of ISG15 and paid special attention to apoptosis. Although not detected in native MIN6 cells, free ISG15 and ISG15 conjugated proteins were both present in dose-dependently increased amounts following stimulation with interferon alpha. As assessed both by caspase 3/7 activity and an annexin V assay, the percentage of apoptotic MIN6 cells (after exposure to the inflammatory cytokines of interleukin-1beta plus interferon gamma or tumor necrosis factor alpha) was decreased by pretreatment with adenovirus-expressing ISG15 and increased by expressing a short hairpin RNA directed against ISG15. In conclusion, ISG15 has an anti-apoptotic effect on MIN6 cells. Thus, promoting ISG15 expression in the pancreatic beta cells could be a potential therapeutic approach for patients with type 1 diabetes.

Journal

  • Endocrine Journal

    Endocrine Journal 61 (9), 883-890, 2014

    The Japan Endocrine Society

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