Transduction of Tat-Superoxide Dismutase into Insulin-producing MIN6N Cells Reduces Streptozotocin-induced Cytotoxicity

  • Choung, In-Soon (Department of Physiology, College of Medicine, Division of Life Sciences, Hallym University) ;
  • Eum, Won-Sik (Department of Genetic Engineering, Division of Life Sciences, Hallym University) ;
  • Li, Ming-Zhen (Department of Physiology, College of Medicine, Division of Life Sciences, Hallym University) ;
  • Sin, Gye-Suk (Department of Physiology, College of Medicine, Division of Life Sciences, Hallym University) ;
  • Kang, Jung-Hoon (Department of Genetic Engineering, Division of Life Sciences, Cheongju University) ;
  • Park, Jin-Seu (Department of Genetic Engineering, Division of Life Sciences, Hallym University) ;
  • Choi, Soo-Young (Department of Genetic Engineering, Division of Life Sciences, Hallym University) ;
  • Kwon, Hyeok-Yil (Department of Physiology, College of Medicine, Division of Life Sciences, Hallym University)
  • Published : 2003.06.21

Abstract

The reactive oxygen species (ROS) are considered to be an important mediator in pancreatic ${\beta}$ cell destruction, thereby triggering the development of insulin-dependent diabetes mellitus. In the present study, HIV-1 Tat-mediated transduction of Cu,Zn-superoxide dismutase (SOD) was investigated to evaluate its protective potential against streptozotocin (STZ)-induced cytotoxicity in insulin-producing MIN6N cells. Tat-SOD fusion protein was successfully delivered into MIN6N cells in a dose-dependent manner and the transduced fusion protein was enzymatically active for 48 h. The STZ induced-cell destruction, superoxide anion radical production, and DNA fragmentation of MIN6N cells were significantly decreased in the cells pretreated with Tat-SOD for 1 h. Furthermore, the transduction of Tat-SOD increased Bcl-2 and heat shock protein 70 (hsp70) expressions in cells exposed to STZ, which might be partly responsible for the effect of Tat-SOD. These results suggest that an increased of free radical scavenging activity by transduction of Tat-SOD enhanced the tolerance of the cell against oxidative stress in STZ-treated MIN6N cells. Therefore, this Tat-SOD transduction technique may provide a new strategy to protect the pancreatic ${\beta}$ cell destruction in ROS-mediated diabetes.

Keywords

References

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