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Corticotropin-Releasing Factor Is Cytoprotective in Xenopus Tadpole Tail: Coordination of Ligand, Receptor, and Binding Protein in Tail Muscle Cell Survival

Departments of Ecology and Evolutionary Biology (G.C.B., R.J.D.), Molecular, Cellular, and Developmental Biology (C.A.K., R.J.D.), and Biological Chemistry and the Molecular and Behavioral Neuroscience Institute (A.F.S.), University of Michigan, Ann Arbor, Michigan 48109

Address all correspondence and requests for reprints to: Robert J. Denver, Ph.D., 830 North University Avenue, 3065C Kraus Natural Science Building, University of Michigan, Ann Arbor, Michigan 48109-1048. E-mail: rdenver{at}umich.edu.

Upon metamorphosis, amphibian tadpoles lose their tails through programmed cell death induced by thyroid hormone (T₃). Before transformation, the tail functions as an essential locomotory organ. The binding protein for the stress neuropeptide corticotropin-releasing factor (CRF; CRF-BP) is strongly up-regulated in the tail of Xenopus tadpoles during spontaneous or T₃-induced metamorphosis. This finding led us to investigate physiological roles for CRF and CRF-BP in tadpole tail. We found CRF, CRF-BP, and functional CRF₁ receptor in tail and CRF and functional CRF₁ receptors, but not CRF-BP, in the tail muscle-derived cell line XLT-15. CRF, acting via the CRF₁ receptor, slowed spontaneous tail regression in explant culture and caused a reduction in caspase 3/7 activity. CRF increased, but stable CRF-BP overexpression decreased, [³H]thymidine incorporation in XLT-15 cells. Overexpression of CRF-BP in vivo accelerated the loss of tail muscle cells during spontaneous metamorphosis. Lastly, exposure of tail explants to hypoxia increased CRF and urocortin 1 but strongly decreased CRF-BP mRNA expression. We show that CRF is expressed in tadpole tail, is up-regulated by environmental stressors, and is cytoprotective. The inhibitory binding protein for CRF is regulated by hormones or by environmental stressors and can modulate CRF bioactivity.

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