Amplification of a reactive oxygen species signal in axotomized retinal ganglion cells
Retinal ganglion cells (RGCs) undergo apoptosis after axonal injury. Elucidation of the sequence of intracellular events proximal to caspase activation may allow development of effective neuroprotective strategies. In this study, we explored the role that reactive oxygen species may have in signalin...
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Published in | Antioxidants & redox signaling Vol. 5; no. 5; p. 629 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
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United States
01.10.2003
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Abstract | Retinal ganglion cells (RGCs) undergo apoptosis after axonal injury. Elucidation of the sequence of intracellular events proximal to caspase activation may allow development of effective neuroprotective strategies. In this study, we explored the role that reactive oxygen species may have in signaling RGC apoptosis after axonal injury. Using the fluorescent probe dihydroethidium, we were able to measure intracellular superoxide anion production. We found that axotomized RGCs exposed to oxidative stress exhibited a secondary superoxide burst. The broad-spectrum caspase inhibitor Z-Val-Ala-DL-Asp-fluoromethyl ketone did not block the burst, suggesting it is proximal to caspase activation, but it was inhibited by cycloheximide, consistent with a requirement for protein synthesis. These results are consistent with RGC axotomy inducing synthesis of one or more proteins that mediate oxidative amplification. This could be an early event in signaling of RGC apoptosis after axonal injury. |
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AbstractList | Retinal ganglion cells (RGCs) undergo apoptosis after axonal injury. Elucidation of the sequence of intracellular events proximal to caspase activation may allow development of effective neuroprotective strategies. In this study, we explored the role that reactive oxygen species may have in signaling RGC apoptosis after axonal injury. Using the fluorescent probe dihydroethidium, we were able to measure intracellular superoxide anion production. We found that axotomized RGCs exposed to oxidative stress exhibited a secondary superoxide burst. The broad-spectrum caspase inhibitor Z-Val-Ala-DL-Asp-fluoromethyl ketone did not block the burst, suggesting it is proximal to caspase activation, but it was inhibited by cycloheximide, consistent with a requirement for protein synthesis. These results are consistent with RGC axotomy inducing synthesis of one or more proteins that mediate oxidative amplification. This could be an early event in signaling of RGC apoptosis after axonal injury. |
Author | Alexejun, Christa N Nguyen, Steve M Levin, Leonard A |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/14580319$$D View this record in MEDLINE/PubMed |
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Snippet | Retinal ganglion cells (RGCs) undergo apoptosis after axonal injury. Elucidation of the sequence of intracellular events proximal to caspase activation may... |
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SubjectTerms | Amino Acid Chloromethyl Ketones - pharmacology Animals Animals, Newborn Axotomy Caspases - metabolism Cell Physiological Phenomena - drug effects Cycloheximide - pharmacology Ethidium - analogs & derivatives Ethidium - pharmacology Hydrogen Peroxide - pharmacology Microscopy, Fluorescence Oxidative Stress - physiology Phosphines - pharmacology Polyethylene Glycols - pharmacology Rats Rats, Long-Evans Reactive Oxygen Species - metabolism Retinal Ganglion Cells - drug effects Retinal Ganglion Cells - metabolism Signal Transduction - drug effects Superoxide Dismutase - pharmacology Superoxides - metabolism Vitamin K 3 - pharmacology |
Title | Amplification of a reactive oxygen species signal in axotomized retinal ganglion cells |
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