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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Clinical Paper Session 02: Nerve Repair/Regeneration
Friday, September 19, 2014 • 9:06–9:13 AM
Category: Basic Science
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