Abstract
Bax is a proapoptotic protein that is required for programmed cell death (PCD) of many neuronal populations. Here we show that, during an early period of retinal PCD and in naturally occurring sensory and motor neuron (MN) death in the spinal cord, Bax delivery results in enhanced death of these neural populations. In contrast, Bax overexpression fails to enhance an early phase of MN death that occurs in the cervical spinal cord, although overexpressed Bax appears to be activated in dying MNs. Bax overexpression does not also affect the survival of immature neurons prior to the PCD period. Taken together, these data provide the first in vivo evidence suggesting that Bax appears to act selectively as an executioner only in neurons undergoing PCD. Furthermore, although Bax appears to mediate the execution pathway for PCD, the effect of Bax overexpression on susceptibility to death differs between different neuronal populations.
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Abbreviations
- DRG:
-
dorsal root ganglion
- EGFP:
-
enhanced green fluorescent protein
- hBax:
-
human Bax
- HSP:
-
heat shock protein
- MN:
-
motor neuron
- PCD:
-
programmed cell death
- STS:
-
staurosporine
- VH:
-
ventral horn
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Acknowledgements
This work is supported by Grant-in-Aid for Scientific Research (14580731, 15590165, 16500223, 17590167) and by the Fukushima Society for the Promotion of Medicine, by the NIH (NS020402) and by a grant from the Robert Packard ALS Center of Johns Hopkins University. We wish to thank the Department of Anatomy for its generous support. We also thank H. Ohuchi for technical assistance, S. H. Hughes for a RSV-derived retroviral plasmid RCASBP(A), B. A. Morgan for an adaptor plasmid Slax13Nco, S. L. Pfaff for a HB9 promoter plasmid, and Y. Tsujimoto for the human bax cDNA.
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Supplementary Information accompanies the paper on Cell Death and Diffrentiation website (http://www.nature.com/cdd).
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Sato, N., Sakuma, C., Sato, Y. et al. Distinct susceptibility of developing neurons to death following Bax overexpression in the chicken embryo. Cell Death Differ 13, 435–445 (2006). https://doi.org/10.1038/sj.cdd.4401760
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DOI: https://doi.org/10.1038/sj.cdd.4401760
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