The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Caspase‐3 Mediated Neuronal Death After Traumatic Brain Injury in Rats
Abstract
Abstract: During programmed cell death, activation of caspase‐3 leads to proteolysis of DNA repair proteins, cytoskeletal proteins, and the inhibitor of caspase‐activated deoxyribonuclease, culminating in morphologic changes and DNA damage defining apoptosis. The participation of caspase‐3 activation in the evolution of neuronal death after traumatic brain injury in rats was examined. Cleavage of pro‐caspase‐3 in cytosolic cellular fractions and an increase in caspase‐3‐like enzyme activity were seen in injured brain versus control. Cleavage of the caspase‐3 substrates DNA‐dependent protein kinase and inhibitor of caspase‐activated deoxyribonuclease and co‐localization of cytosolic caspase‐3 in neurons with evidence of DNA fragmentation were also identified. Intracerebral administration of the caspase‐3 inhibitor N‐benzyloxycarbonyl‐Asp‐Glu‐Val‐Asp‐fluoromethyl ketone (480 ng) after trauma reduced caspase‐3‐like activity and DNA fragmentation in injured brain versus vehicle at 24 h. Treatment with N‐benzyloxycarbonyl‐Asp‐Glu‐Val‐Asp‐fluoromethyl ketone for 72 h (480 ng/day) reduced contusion size and ipsilateral dorsal hippocampal tissue loss at 3 weeks but had no effect on functional outcome versus vehicle. These data demonstrate that caspase‐3 activation contributes to brain tissue loss and downstream biochemical events that execute programmed cell death after traumatic brain injury. Caspase inhibition may prove efficacious in the treatment of certain types of brain injury where programmed cell death occurs.
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Cites
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KOCHANEK, P. M., MARION, D. W., ZHANG, W., SCHIDING, J. K., WHITE, M., PALMER, A. M., CLARK, R. S. B., O'MALLEY, M. E., STYREN, S. D., HO, C., et al. (1995) · Journal of Neurotrauma · doi:10.1089/neu.1995.12.1015 · Cited by 203 · cited 1×
“After removal of the bone flap, injury was produced using the CCI device as previously described with minor modification (Kochanek et al., 1995).”
MethodSelf-citation
Cited by
Loane, D. J., & Faden, A. I. (2010) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2010.09.005 · Cited by 574
Molecular mechanisms of cognitive dysfunction following traumatic brain injury
Walker, K. R., & Tesco, G. (2013) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2013.00029 · Cited by 265
DeWitt, D. S., & Prough, D. S. (2003) · Journal of Neurotrauma · doi:10.1089/089771503322385755 · Cited by 195
Sex differences in mitochondrial (dys)function: Implications for neuroprotection
Demarest, T. G., & McCarthy, M. M. (2015) · Journal of Bioenergetics and Biomembranes · doi:10.1007/s10863-014-9583-7 · Cited by 192
Mitochondria-associated microRNAs in rat hippocampus following traumatic brain injury
Wang, W.-X., Visavadiya, N. P., Pandya, J. D., Nelson, P. T., Sullivan, P. G., & Springer, J. E. (2015) · Experimental Neurology · doi:10.1016/j.expneurol.2014.12.018 · Cited by 134
Cytochrome c release and caspase activation after traumatic brain injury
Sullivan, P. G., Keller, J. N., Bussen, W. L., & Scheff, S. W. (2002) · Brain Research · doi:10.1016/s0006-8993(02)02968-2 · Cited by 129
Abrahamson, E. E., Ikonomovic, M. D., Ciallella, J. R., Hope, C. E., Paljug, W. R., Isanski, B. A., Flood, D. G., Clark, R. S. B., & DeKosky, S. T. (2006) · Experimental Neurology · doi:10.1016/j.expneurol.2005.10.011 · Cited by 90
Self-citationTraumatic brain injury causes frontotemporal dementia and TDP-43 proteolysis
Wang, H.-K., Lee, Y.-C., Huang, C.-Y., Liliang, P.-C., Lu, K., Chen, H.-J., Li, Y.-C., & Tsai, K.-J. (2015) · Neuroscience · doi:10.1016/j.neuroscience.2015.05.013 · Cited by 72
Depletion of GGA1 and GGA3 Mediates Postinjury Elevation of BACE1
Walker, K. R., Kang, E. L., Whalen, M. J., Shen, Y., & Tesco, G. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.5491-11.2012 · Cited by 66
Evaluation of apoptosis in cerebrospinal fluid of patients with severe head injury
Uzan, M., Erman, H., Tanriverdi, T., Sanus, G. Z., Kafadar, A., & Uzun, H. (2006) · Acta Neurochirurgica · doi:10.1007/s00701-006-0887-1 · Cited by 61
A Mapping Study of Caspase-3 Activation Following Acute Spinal Cord Contusion in Rats
McEwen, M. L., & Springer, J. E. (2005) · Journal of Histochemistry & Cytochemistry · doi:10.1369/jhc.4a6467.2005 · Cited by 48
Kim, W., Ma, L., Lomoio, S., Willen, R., Lombardo, S., Dong, J., Haydon, P. G., & Tesco, G. (2018) · Molecular Neurodegeneration · doi:10.1186/s13024-018-0239-7 · Cited by 32
Beneficial effect of amyloid beta after controlled cortical impact
Mannix, R. C., Zhang, J., Berglass, J., Qui, J., & Whalen, M. J. (2013) · Brain Injury · doi:10.3109/02699052.2013.771797 · Cited by 19
Metadata
- Authors
- Clark, R. S. B., Kochanek, P. M., Watkins, S. C., Chen, M., Dixon, C. E., Seidberg, N. A., Melick, J., Loeffert, J. E., Nathaniel, P. D., Jin, K. L., & Graham, S. H.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2000-02
- Volume
- 74
- Issue
- 2
- Pages
- 740-753
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2022647670
- Cited by
- 405
- References
- 2
- FWCI
- 15.58
- Type
- journal article
- Language
- en
- Open access
- closed
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