Share
Available online 3 September 2010.
Kindly supplied by Juan Carlos Baiges through Internaf and FAPG
Abstract
Reactive oxygen species (ROS) actively contribute to the development of a number of human diseases including ischemia. In response to oxidative stress, frataxin has a significant ability to improve cell survival though its biological function is unclear in relation to ischemia. To explore frataxin's role in protecting against ischemic cell death, we constructed PEP-1-Frataxin cell-permeable fusion protein. In a dose- and time-dependent manner PEP-1-Frataxin rapidly transduced into astrocyte cells and protected them against oxidative stress-induced cell death.
Further, using an animal model, immunohistochemical analysis revealed that PEP-1-Frataxin prevented neuronal cell death in the CA1 region of the hippocampus induced by transient forebrain ischemia. These results demonstrate that transduced PEP-1-Frataxin protects against cell death in vitro and in vivo, suggesting that transduction of PEP-1-Frataxin could be useful as a therapeutic agent for various human diseases related to oxidative stress.
Authors:
Mi Jin Kima, 1, Dae Won Kima, 1, Ki-Yeon Yoob, 1, Eun Jeong Sohna, Hoon Jae Jeonga, Hye Won Kanga, Min Jea Shina, Eun Hee Ahna, Jae Jin Ana, Soon Won Kwona, Young Nam Kima, Moo Ho Wonb, Sung-Woo Choc, Jinseu Parka, Won Sik Euma, and Soo Young Choia
a Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon 200-702, Republic of Korea
b Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon 200-702, Republic of Korea
c Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 138-736, Republic of Korea
| Comments |
|
