Inhibition of programmed cell death by cyclosporin.
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.
Department of Biochemistry and Molecular Biology, Texas Tech University Health Sciences Center, School of Medicine, Lubbock 79430.
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Little
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Flores
D000818:Animals; D017209:Apoptosis / Q000187:drug effects* / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D002738:Chloroquine / Q000494:pharmacology; D016572:Cyclosporine / Q000494:pharmacology*; D005033:Ethylmaleimide / Q000494:pharmacology; D008565:Membrane Proteins / Q000378:metabolism; D011892:Rana catesbeiana; D013481:Superoxides / Q000378:metabolism; D014284:Triiodothyronine / Q000494:pharmacology
D008565:Membrane Proteins; D014284:Triiodothyronine; D013481:Superoxides; D016572:Cyclosporine; D002738:Chloroquine; D005033:Ethylmaleimide