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Prevention of vertebrate neuronal death by the crmA gene
V Gagliardini1, P A Fernandez, R K Lee
1Cardiovascular Research Center, Massachusetts General Hospital, Charlestown 02129.
Abstract:
Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of CED-3, a protein required for programmed cell death in the nematode Caenorhabditis elegans. The activity of ICE can be specifically inhibited by the product of crmA, a cytokine response modifier gene encoded by cowpox virus. Microinjection of the crmA gene into chicken dorsal root ganglion neurons was found to prevent cell death induced by deprivation of nerve growth factor. Thus, ICE is likely to participate in neuronal death in vertebrates.
Insights
Interleukin-1 beta converting enzyme (ICE) participates in programmed cell death. Inhibiting ICE with the cowpox virus crmA gene prevented nerve growth factor deprivation-induced neuronal death, suggesting ICE
Area of Science:
- Molecular Biology
- Neuroscience
- Cell Biology
Background:
- Interleukin-1 beta converting enzyme (ICE) is a mammalian homolog of Caenorhabditis elegans CED-3.
- CED-3 is essential for programmed cell death in nematodes.
- Cowpox virus encodes a cytokine response modifier gene (crmA) that inhibits ICE activity.
Purpose of the Study:
- To investigate the role of ICE in vertebrate neuronal cell death.
- To determine if crmA can prevent neuronal apoptosis.
Main Methods:
- Microinjection of the crmA gene into chicken dorsal root ganglion neurons.
- Induction of cell death by deprivation of nerve growth factor.
Main Results:
- Microinjection of crmA successfully inhibited ICE activity.
- crmA gene delivery prevented nerve growth factor deprivation-induced neuronal cell death.
Conclusions:
- ICE is implicated in programmed neuronal cell death in vertebrates.
- Targeting ICE may offer therapeutic strategies for neurodegenerative diseases.