We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Transduced Human Copper Chaperone for Cu,Zn-SOD (PEP-1-CCS) Protects Against Neuronal Cell Death.
- Authors
Soo Hyun Choi; Dae Won Kim; So Young Kim; Jae Jin An; Sun Hwa Lee; Hee Soon Choi; Eun Jung Sohn; Seok-Il Hwang; Moo Ho Won; Tae-Cheon Kang; Hyung Joo Kwon; Jung Hoon Kang; Sung-Woo Cho; Jinseu Park; Won Sik Eum; Soo Young Choi
- Abstract
Reactive oxygen species (ROS) contribute to the development of various human diseases. Cu,Zn-superoxide dismutase (SOD) is one of the major means by which cells counteract the deleterious effects of ROS. SOD activity is dependent upon bound copper ions supplied by its partner metallochaperone protein, copper chaperone for SOD (CCS). In the present study, we investigated the protective effects of PEP-1-CCS against neuronal cell death and ischemic insults. When PEP-1-CCS was added to the culture medium of neuronal cells, it rapidly entered the cells and protected them against paraquat-induced cell death. Moreover, transduced PEP-1-CCS markedly increased endogenous SOD activity in the cells. Immunohistochemical analysis revealed that it prevented neuronal cell death in the hippocampus in response to transient forebrain ischemia. These results suggest that CCS is essential to activate SOD, and that transduction of PEP-1-CCS provides a potential strategy for therapeutic delivery in various human diseases including stroke related to SOD or ROS.
- Publication
Molecules & Cells (Springer Nature), 2005, Vol 20, Issue 3, p401
- ISSN
1016-8478
- Publication type
Article
- DOI
10.1016/s1016-8478(23)13245-6