Mst3b Promote Spinal Cord Neurons Regeneration By Phosphorylating LIMK1/Cofilin In Spinal Cord Injury Rats

Spinal cord injury (SCI) is a clinical common disease, and the therapies for SCI has limited therapeutic effect, due to low intrinsic regenerative capacity of injured central neurons and inhibitory extrinsic environment, so searching for a key molecule promoting damage neurons in the spinal cord is a hot spot in the present study. Previous study showed that Mst3b, a neuron-specific expression kinase protein, is essential for axon outgrowth in several neurons and beneficial for neurodegeneration and nerve injury disease, but rarely reported in spinal cord injury research. To research whether Mst3b promote SCI recovering and the mechanisms, firstly, we detected Mst3b expression in different injury periods spinal cord. The results showed that Mst3b was neuron-specific expression and the quantity was significantly up-regulated in SCI rats. Secondly, we studied Mst3b role for recovery of spinal cord neurons and SCI rats, in vivo and in vitro, by increasing or down-regulation Mst3b expression through adenovirus (ADV) infections.The research illustrated that over-expression Mst3b can facilitate spinal cord neurons outgrowth and SCI rats recovery, but down-regulation of Mst3b levels, we found the adverse effects. Finally, to prove whether Mst3b promote neurons outgrowth by regulating growth cone skeleton, we precipitated Mst3b and detecting the activity level by immunblotting indicated proteins. In the present study, we found that Mst3b can combine with small G protein Racl and transphosphorylation Cofilin, a depolymerization factor of F-actin, regulating growth cone skeleton driving outgrowth of neurons. Thus, the present research supplied a new therapy target for SCI with experimental support.