Transduction of Tat-Superoxide Dismutase into Insulin-producing MIN6N Cells Reduces Streptozotocin-induced Cytotoxicity.
- Author:
In Soon CHOUNG
1
;
Won Sik EUM
;
Ming Zhen LI
;
Gye Suk SIN
;
Jung Hoon KANG
;
Jinseu PARK
;
Soo Young CHOI
;
Hyeok Yil KWON
Author Information
1. Department of Physiology, College of Medicine, Hallym University, Chuncheon 200-702, Korea. hykwon@hallym.ac.kr
- Publication Type:Original Article
- Keywords:
Diabetes;
Tat-mediated transduction;
Superoxide dismutase;
ROS;
Insulin-producing cells
- MeSH:
Diabetes Mellitus, Type 1;
DNA Fragmentation;
HIV-1;
HSP70 Heat-Shock Proteins;
Insulin-Secreting Cells;
Oxidative Stress;
Reactive Oxygen Species;
Streptozocin;
Superoxide Dismutase;
Superoxides
- From:The Korean Journal of Physiology and Pharmacology
2003;7(3):163-168
- CountryRepublic of Korea
- Language:English
-
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.
