Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
1914522 | Journal of the Neurological Sciences | 2010 | 6 Pages |
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.
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Authors
Mi Jin Kim, Dae Won Kim, Ki-Yeon Yoo, Eun Jeong Sohn, Hoon Jae Jeong, Hye Won Kang, Min Jea Shin, Eun Hee Ahn, Jae Jin An, Soon Won Kwon, Young Nam Kim, Moo Ho Won, Sung-Woo Cho, Jinseu Park, Won Sik Eum, Soo Young Choi,