Recent data has shown that preservation of the neuromuscular junction after traumatic
nerve injury helps to improve functional recovery with surgical repair. As such, we
sought to explore additional pathways that may augment this response. Wnt signaling
proteins play an important role in the development and the maintenance of the neuromuscular
junction (NMJ). Specifically, Wnt3a has been shown to inhibit agrin-induced acetylcholine
receptor (AChR) clustering by suppressing Rapsyn expression via ß-catenin dependent
signaling. Based on this, we hypothesized that Wnt3a and ß-catenin are associated
with the NMJ destabilization following traumatic nerve injury.
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References
- Matrix metalloproteinase 3 deletion preserves denervated motor endplates after traumatic nerve injury.Ann Neurol. 2013; 73: 210-223
- Wnt/beta-catenin signaling suppresses Rapsyn expression and inhibits acetylcholine receptor clustering at the neuromuscular junction.J Biol Chem. 2008; 283: 21668-21675
- A sensitive and bright single-cell resolution live imaging reporter of Wnt/ß-catenin signaling in the mouse.BMC Dev Biol. 2010; 10: 121
Article info
Publication history
Paper 17
Footnotes
Clinical Paper Session 02: Nerve Repair/Regeneration
Friday, September 19, 2014 • 9:06–9:13 AM
Category: Basic Science
Keyword: Nerve
Identification
Copyright
© 2014 Published by Elsevier Inc.
