The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Delayed treatment with a p53 inhibitor enhances recovery in stroke brain
Abstract
Objective: Cerebral ischemia can activate endogenous reparative processes, such as proliferation of endogenous neural progenitor cells (NPCs) in the subventricular zone (SVZ). Most of these new cells die shortly after injury. The purpose of this study was to examine a novel strategy for treatment of stroke at 1 week after injury by enhancing the survival of ischemia‐induced endogenous NPCs in SVZ. Methods: Adult rats were subjected to a 90‐minutes middle cerebral artery occlusion. A p53 inhibitor pifithrin‐α (PFT‐α) was administered to stroke rats from days 6 to 9 after middle cerebral artery occlusion. Locomotor behavior was measured using an activity chamber. Proliferation, survival, migration, and differentiation of endogenous NPCs were examined using quantitative reverse transcription polymerase chain reaction, terminal deoxynucleotidyl transferase‐mediated dUTP nick‐end labeling, and immunohistochemistry. Results: PFT‐α enhanced functional recovery as assessed by a significant increase in multiple behavioral measurements. Delayed PFT‐α treatment had no effect on the cell death processes in the lesioned cortical region. However, it enhanced the survival of SVZ progenitor cells, and promoted their proliferation and migration. PFT‐α inhibited the expression of a p53‐dependent proapoptotic gene, termed PUMA (p53‐upregulated modulator of apoptosis), within the SVZ of stroke animals. The enhancement of survival/proliferation of NPCs was further found in SVZ neurospheres in tissue culture. PFT‐α dose‐dependently increased the number and size of new neurosphere formation. Interpretation: Delayed treatment with a p53 inhibitor PFT‐α is able to modify stroke‐induced endogenous neurogenesis and improve the functional recovery in stroke animals. Ann Neurol 2009;65:520–530
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“In addition, ischemia at different organ sites can provoke p53-dependent apoptosis that contributes to the resultant pathologies, as in the cases of stroke and myocardial infarction (Liu et al., 2006; Luo et al., 2009; Morrison et al., 2003).”
From p53 at a glance (2010) · cites this paper as Luo et al., 2009
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Neuronal replacement from endogenous precursors in the adult brain after stroke
Arvidsson, A., Collin, T., Kirik, D., Kokaia, Z., & Lindvall, O. (2002) · Nature Medicine · doi:10.1038/nm747 · Cited by 2,799
APAF1 is a key transcriptional target for p53 in the regulation of neuronal cell death
Fortin, A., Cregan, S. P., MacLaurin, J. G., Kushwaha, N., Hickman, E. S., Thompson, C. S., Hakim, A., Albert, P. R., Cecconi, F., Helin, K., et al. (2001) · The Journal of Cell Biology · doi:10.1083/jcb.200105137 · Cited by 194
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Cited by
Metabolic control of cell death
Green, D. R., Galluzzi, L., & Kroemer, G. (2014) · Science · doi:10.1126/science.1250256 · Cited by 647
Brady, C. A., & Attardi, L. D. (2010) · Journal of Cell Science · doi:10.1242/jcs.064501 · Cited by 403
Wang, P., Xu, T., Guan, Y., Tian, W., Viollet, B., Rui, Y., Zhai, Q., Su, D., & Miao, C. (2011) · Annals of Neurology · doi:10.1002/ana.22236 · Cited by 288
Metadata
- Authors
- Luo, Y., Kuo, C., Shen, H., Chou, J., Greig, N. H., Hoffer, B. J., & Wang, Y.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2009-05
- Volume
- 65
- Issue
- 5
- Pages
- 520-530
- ISSN
- 0364-5134
- 1531-8249
- Cited by
- 94
- References
- 2
- Language
- en
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- Luo, Y., Kuo, C., Shen, H., Chou, J., Greig, N. H., Hoffer, B. J., & Wang, Y. (2009). Delayed treatment with a p53 inhibitor enhances recovery in stroke brain. Annals of Neurology. https://doi.org/10.1002/ana.21592
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