The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Cell cycle activation contributes to post-mitotic cell death and secondary damage after spinal cord injury
Abstract
Spinal cord injury (SCI) causes delayed secondary biochemical alterations that lead to tissue loss and associated neurological dysfunction. Up-regulation of cell cycle proteins occurs in both neurons and glia after SCI and may contribute to these changes. The present study examined the role of cell cycle activation on secondary injury after severe SCI in rat. SCI caused cell cycle protein up-regulation associated with neuronal and oligodendroglial apoptosis, glial scar formation and microglial activation. Treatment with the cell cycle inhibitor flavopiridol reduced cell cycle protein induction and significantly improved functional recovery versus vehicle-treated controls at 21 and 28 days post-injury. Treatment also significantly reduced lesion volume, as measured by MRI and histology, decreased astrocytic reactivity, attenuated neuronal and oligodendroglial apoptosis and reduced the production of factors associated with microglial activation. Thus, flavopiridol treatment improves outcome after SCI by inhibiting cell cycle pathways, resulting in beneficial multifactorial actions on neurons and glia.
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“In fact, available evidence indicates that EZH2, E2F2, E2F3, and CCND3 become upregulated in the damaged spinal cord [90,91,92] and induce neuronal death during SCI’s secondary damage [9,90,93].”
From MicroRNA-138-5p Targets Pro-Apoptotic Factors and Favors Neural Cell Survival: Analysis in the Injured Spinal Cord (2022) · cites this paper as [93]
Citations
Cites
Chapter 4 Cell death in models of spinal cord injury
Beattie, M. S., Hermann, G. E., Rogers, R. C., & Bresnahan, J. C. (2002) · Progress in Brain Research · doi:10.1016/s0079-6123(02)37006-7 · Cited by 453
Temporal–Spatial Pattern of Acute Neuronal and Glial Loss after Spinal Cord Contusion
Grossman, S. D., Rosenberg, L. J., & Wrathall, J. R. (2001) · Experimental Neurology · doi:10.1006/exnr.2001.7628 · Cited by 310
Cited by
Sorted by citations
Loane, D. J., & Faden, A. I. (2010) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2010.09.005 · Cited by 574
Self-citationFlavopiridol reduces the impedance of neural prostheses in vivo without affecting recording quality
Purcell, E. K., Thompson, D. E., Ludwig, K. A., & Kipke, D. R. (2009) · Journal of Neuroscience Methods · doi:10.1016/j.jneumeth.2009.06.026 · Cited by 62
Cdk5 and the non-catalytic arrest of the neuronal cell cycle
Zhang, J., & Herrup, K. (2008) · Cell Cycle · doi:10.4161/cc.7.22.7045 · Cited by 44
Inhibition of amyloid precursor protein secretases reduces recovery after spinal cord injury
Pajoohesh-Ganji, A., Burns, M. P., Pal-Ghosh, S., Tadvalkar, G., Hokenbury, N. G., Stepp, M. A., & Faden, A. I. (2014) · Brain Research · doi:10.1016/j.brainres.2014.02.049 · Cited by 29
Self-citationMaza, R. M., Barreda-Manso, M. A., Reigada, D., Silván, Á., Muñoz-Galdeano, T., Soto, A., del Águila, Á., & Nieto-Díaz, M. (2022) · Biomedicines · doi:10.3390/biomedicines10071559 · Cited by 12
Metadata
- Authors
- Byrnes, K. R., Stoica, B. A., Fricke, S., Di Giovanni, S., & Faden, A. I.
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-04-05
- Volume
- 130
- Issue
- 11
- Pages
- 2977-2992
- ISSN
- 0006-8950
- 1460-2156
- Cited by
- 139
- References
- 2
- Language
- en
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- CoChat. (2026). Citation check: Cell cycle activation contributes to post-mitotic cell death and secondary damage after spinal cord injury. https://app.cochat.ai/papers/10.1093/brain/awm179
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- Byrnes, K. R., Stoica, B. A., Fricke, S., Di Giovanni, S., & Faden, A. I. (2007). Cell cycle activation contributes to post-mitotic cell death and secondary damage after spinal cord injury. Brain. https://doi.org/10.1093/brain/awm179
