PUBLICATION

E2F4 Promotes Neuronal Regeneration and Functional Recovery after Spinal Cord Injury in Zebrafish

Authors
Sasagawa, S., Nishimura, Y., Hayakawa, Y., Murakami, S., Ashikawa, Y., Yuge, M., Okabe, S., Kawaguchi, K., Kawase, R., Tanaka, T.
ID
ZDB-PUB-160601-6
Date
2016
Source
Frontiers in pharmacology   7: 119 (Journal)
Registered Authors
Tanaka, Toshio
Keywords
DREAM complex, E2F4, comparative transcriptome analysis, spinal cord injury, systems pharmacology, zebrafish
MeSH Terms
none
PubMed
27242526 Full text @ Front Pharmacol
Citation
Sasagawa, S., Nishimura, Y., Hayakawa, Y., Murakami, S., Ashikawa, Y., Yuge, M., Okabe, S., Kawaguchi, K., Kawase, R., Tanaka, T. (2016) E2F4 Promotes Neuronal Regeneration and Functional Recovery after Spinal Cord Injury in Zebrafish. Frontiers in pharmacology. 7:119.
Abstract
Mammals exhibit poor recovery after spinal cord injury (SCI), whereas non-mammalian vertebrates exhibit significant spontaneous recovery after SCI. The mechanisms underlying this difference have not been fully elucidated; therefore, the purpose of this study was to investigate these mechanisms. Using comparative transcriptome analysis, we demonstrated that genes related to cell cycle were significantly enriched in the genes specifically dysregulated in zebrafish SCI. Most of the cell cycle-related genes dysregulated in zebrafish SCI were down-regulated, possibly through activation of e2f4. Using a larval zebrafish model of SCI, we demonstrated that the recovery of locomotive function and neuronal regeneration after SCI were significantly inhibited in zebrafish treated with an E2F4 inhibitor. These results suggest that activation of e2f4 after SCI may be responsible, at least in part, for the significant recovery in zebrafish. This provides novel insight into the lack of recovery after SCI in mammals and informs potential therapeutic strategies.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
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