Vimentin Inhibits Neuronal Apoptosis After Spinal Cord Injury by Enhancing Autophagy

Aims: Neuron death is caused primarily by apoptosis after spinal cord injury (SCI). Autophagy, as a cellular response, can maintain cellular homeostasis to reduce apoptosis. We aimed to investigate the effect and the mechanism of vimentin knockdown on autophagy and neural recovery after SCI.

Methods: The SD rats with T10 complete transection as SCI model were used. The vimentin RNAi adenovirus was constructed and transplanted into T10 rats with total transection injury of the spinal cord, and the recovery of neurological and motor functions after SCI was evaluated by BBB score, footprint analysis, electrophysiological tests, and immunofluorescence staining. Protein and gene expression were assessed by Western blotting, CO-IP, q-PCR, and immunofluorescence. In addition, neuron-like PC12 cells were infected with adenovirus to further elucidate the effect of vimentin on autophagy and the molecular mechanism of neuronal apoptosis after SCI.

Results: Inhibition of SCI induced-vimentin upregulation improved motor function, enhanced the recovery of autophagy flux, and reduced neuronal apoptosis. Notably, this may be related to the formation of vimentin-14-3-3-Beclin1 complex and PI3K class III complex.

Conclusion: Our results suggest that inhibition of vimentin expression may enhance autophagy and anti-apoptosis in neurons after SCI by affecting the formation of the vimentin-14-3-3-Beclin1 complex, thereby promoting neuronal recovery.