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Inhibition of programmed cell death by cyclosporin
1Department of Biochemistry and Molecular Biology, Texas Tech University Health Sciences Center, School of Medicine, Lubbock 79430.
Abstract:
1. Apoptosis is generally believed to occur as a consequence of activation of an internal, genetically controlled, program in the dying cells. 2. We have proposed an alternative hypothesis that, in hormone-induced apoptosis, the active participation of dying cells in the death process may be limited to expressing surface proteins that permit identification of cells destined to die by cytotoxic effector cells. 3. We investigated the effects of the immunosuppressant, cyclosporin, and the lysosomotropic agents, chloroquine and N-ethyl maleimide on thyroid hormone-induced regression of the bullfrog tadpole tail. 4. All three substances blocked regression. These results suggest that patency of the intracellular protein trafficking machinery is essential for programmed cell death in our system.
Insights
This study challenges the traditional view of apoptosis, suggesting cell death may involve external identification rather than internal programming. Blocking protein trafficking inhibited hormone-induced cell death in tadpole tails.
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- Apoptosis is traditionally viewed as an internally programmed cell death process.
- An alternative hypothesis suggests dying cells may signal for external identification by cytotoxic cells.
- Hormone-induced apoptosis in specific systems may involve different mechanisms.
Purpose of the Study:
- To investigate the role of intracellular protein trafficking in hormone-induced apoptosis.
- To test the hypothesis that dying cells actively participate in their own demise.
- To explore the effects of specific inhibitors on programmed cell death.
Main Methods:
- Utilized thyroid hormone to induce apoptosis in bullfrog tadpole tails.
- Administered cyclosporin, chloroquine, and N-ethyl maleimide to block protein trafficking.
- Observed the effects of these substances on tadpole tail regression.
Main Results:
- Cyclosporin, chloroquine, and N-ethyl maleimide all blocked thyroid hormone-induced tail regression.
- These findings indicate that intracellular protein trafficking is crucial for this form of programmed cell death.
- The results support the idea that active cellular machinery is involved in apoptosis.
Conclusions:
- Intracellular protein trafficking machinery is essential for programmed cell death in the bullfrog tadpole tail system.
- The active participation of dying cells may be more complex than previously assumed.
- Further research is needed to fully elucidate the mechanisms of hormone-induced apoptosis.