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Wnt/β-catenin signaling promotes regeneration after adult zebrafish spinal cord injury
Unlike mammals, zebrafish can regenerate their injured spinal cord and regain control of caudal tissues. It was recently shown that Wnt/β-catenin signaling is necessary for spinal cord regeneration in the larval zebrafish. However, the molecular mechanisms of regeneration may or may not be conserved...
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Published in: | Biochemical and biophysical research communications 2016-09, Vol.477 (4), p.952-956 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Unlike mammals, zebrafish can regenerate their injured spinal cord and regain control of caudal tissues. It was recently shown that Wnt/β-catenin signaling is necessary for spinal cord regeneration in the larval zebrafish. However, the molecular mechanisms of regeneration may or may not be conserved between larval and adult zebrafish. To test this, we assessed the role of Wnt/β-catenin signaling after spinal cord injury in the adult zebrafish. We show that Wnt/β-catenin signaling is increased after spinal cord injury in the adult zebrafish. Moreover, overexpression of Dkk1b inhibited Wnt/β-catenin signaling in the regenerating spinal cord of adult zebrafish. Dkk1b overexpression also inhibited locomotor recovery, axon regeneration, and glial bridge formation in the injured spinal cord. Thus, our data illustrate a conserved role for Wnt/β-catenin signaling in adult and larval zebrafish spinal cord regeneration.
•Wnt/β-catenin signaling is increased after spinal cord injury in adult zebrafish.•Dkk overexpression inhibits Wnt/β-catenin signaling in the injured spinal cord.•Dkk overexpression inhibits locomotor recovery after spinal cord injury.•Dkk overexpression inhibits axon regeneration & glial bridge formation. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2016.07.006 |