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.
Keywords
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Article info
Publication history
Published online: September 06, 2010
Accepted:
August 9,
2010
Received in revised form:
August 1,
2010
Received:
June 10,
2010
Identification
Copyright
© 2010 Elsevier B.V. Published by Elsevier Inc. All rights reserved.
