Snx27 Deletion Promotes Functional Recovery Of Mice From Spinal Cord Injury By Neuroprotection And Reduces Microglia/macrophage Proliferation

Objective This study to explore its importance of SNX27 in the pathogenesis after spinal cord injury(SCI)through the detection of its expression in time and space.We detect the possible mechanism of SNX27 invovled in the neuronal apoptosis and activation of glial cell hyperplasia after spinal cord injury.So as to provide new clinical treatment after spinal cord injury treatment.Methods Firstly,we constructed a spinal cord injury model in mice,and detected the expression of SNX27 after spinal cord injury by Western blotting and immunofluorescence.Secondly,the Snx27+/+ mice and Snx27+/-mice are used to detect the effect of SNX27 in functional recovery and corticospinal tract regeneration through behavioral test and BDA tract.At the same time by Western blotting and immunofluorescence,we detect the apoptosis of neuron and proliferation of glial cells,in order to explore the impaction of loss of SNX27 invovled in neurons death and proliferation of glial after injury.Conclusion1.Expression of SNX27 is up-regulated in the injured spinal cord and reached its peak on day 7 post-injury;2.SNX27 haploinsufficiency promotes functional recovery after SCI3.SNX27 haploinsufficiency increases axon regeneration after SCI.4.SNX27 haploinsufficiency prevents neuronal death and caspase-3 activation after SCI5.SNX27 haploinsufficiency does not influence gliosis after SCI6.SNX27 haploinsufficiency reduces the infiltration and activation of macrophage/microglia7.SNX27 haploinsufficiency suppresses the proliferation of microglia/macrophage after SCIConclusion Snx27 deletion promotes functional recovery of mice from spinal cord injury by neuroprotection and reduces macrophage/microglia proliferation...