期刊
NEUROSCIENCE LETTERS
卷 453, 期 3, 页码 182-185出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2009.02.020
关键词
Cytochrome c; Apoptosis-inducing factor; Ischemic insult
资金
- NIH [2P01 NS37520]
Apoptosis arises from neuronal damage following an ischemic insult. Apoptosis-inducing factor (AIF) is a protein released from mitochondria in response to pro-apoptotic signals which then translocates to the nucleus and triggers DNA fragmentation. In parallel with this, pro-apoptotic signals cause the release of cytochrome c from mitochondria, activating caspase-dependent apoptosis. During post-ischemic reperfusion, reactive oxygen species (ROS) are formed in excess in mitochondria and can play a role in initiating apoptosis. In cultures, ROS are formed during post oxygen glucose deprivation (OGD) normoxia/normoglycemia that is used as a model for ischemia. In this study, we delivered viral vectors to overexpress antioxidants (GPX, catalase, CuZnSCD, or MnSOD) in mixed cortical cultures, in order to investigate the effects of ROS-reduction on the release of cytochrome c and AIF Overexpression of MnSOD, CuZnSOD, catalase or GPX all prevented AT translocation from mitochondria to the nucleus. Potentially, this could reflect broadly non-specific protection due to reducing ROS load. Arguing against this, overexpression of the same antioxidants did not inhibit cytochrome c release. These findings suggest a specific interaction between ROS formation and the caspase-independent route of apoptosis. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
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