Polyethylene Glycol Inhibits Apoptotic Cell Death Following Traumatic Spinal Cord Injury.
From: Center for Paralysis Research, Department of Medical Sciences, School of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA.
Brain research
- Publish Date: Jun 2007
- ISSN: 0006-8993
- Volume: 1155
- Issue:
- Pages: 10-6
- Medium: Print
- Language: English
- Citation (JAMA): Luo Jian, Shi Riyi, et al. Polyethylene Glycol Inhibits Apoptotic Cell Death Following Traumatic Spinal Cord Injury.. Brain Res. Jun 2007;1155:10-6
Abstract
We have previously shown that local administration of polyethylene glycol (PEG, MW: 2000 Da, 50% by weight), a known membrane repair agent, immediately after trauma in guinea pig spinal cord repairs neuronal membrane disruptions and reduces oxidative injury. Here we report that a similar application of PEG resulted in marked decreases in apoptotic cell death and caspase-3 activity. We suggest that PEG may suppress apoptosis through interactions with mitochondria. This is based on our current findings that in isolated mitochondria, PEG improves mitochondrial function and reduces the release of cytochrome c, a pro-apoptotic cell death factor. This hypothesis is further supported by our previous observation that PEG enters injured cells after spinal cord injury, placing PEG in a position to directly interact with mitochondria. In summary, we conclude that PEG reduces both necrosis and apoptosis through two distinct yet synergistic pathways: repair of disrupted plasma membranes and protection of mitochondria through direct interaction.
Mesh Headings (Keywords): Animals, Apoptosis, Calcium, Caspase 3, Cell Death, Cytochromes c, Glutathione, Guinea Pigs, Mitochondria, Polyethylene Glycols, Spinal Cord Injuries
Check for Full Text / PubMed Unique Identifier (PMID): 17512912
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