Mst3b promotes spinal cord neuronal regeneration by promoting growth cone branching out in spinal cord injury rats.

Spinal cord injury is a severe clinical problem, and research searching activity molecular that can promote spinal cord injury repairing is very prevalent. Mst3b can promote repair of damaged peripheral nerves and the optic nerve, but has been rarely reported in spinal cord injury research. Through detecting its expression in different periods of injured spinal cord, we found that the expression of Mst3b was significantly upregulated in injured spinal cord neurons. Increasing Mst3b expression using adenovirus in vivo and in vitro promoted axonal regeneration of spinal cord neurons, which led to behavioral and electrophysiological improvement. Downregulation of Mst3b level had the adverse effects. Increasing Mst3b expression in PC12 cells resulted in an elevation of P42/44(MAPK) and LIMK/Cofilin activation. These results identified Mst3b as a powerful regulator for promoting spinal cord injury recovery through the P42/44(MAPK) and LIMK/Cofilin signaling pathways.