The Impact of Compression Duration on the RhoA, P75, S100 Expression in Spinal Cord Injury in Rat

 Compression of the spinal cord induces alterations in protein expression of neurons and glia cells, which in turn triggers a cascade of pathophysiologic events. It's well-documented that activation of inhibitory proteins following spinal cord injury stimulates activation of the RhoA via neurotrophin receptor p75 (p75NTR), which causes promotion of apoptotic cell death and inhibiting axon outgrowth. Elucidating the underlying factors driving the expressions during sustained compression is important to develop new therapeutic strategies.

 To investigate the impact of compression duration on the RhoA, P75, and S100 expression in spinal cord injury model in rats.

 We investigated the impact of compression duration on the expression of RhoA, p75NTR, and S100β in rats with spinal cord injury (SCI). Initially, rats were subjected to SCI using an aneurism clip at the T9 vertebrae lamina for 3 sec or 10 min. Sham group was subjected to laminectomy only. We compared spinal cord histopathology at 3 and 14 days after injury for both short and prolonged compressive surgery groups. At the respective scarify times points, the rats were sacrificed, and the pathology of the injury was studied using light microscopy and immunohistochemistry.

 We found a greater expression level of p75NTR, S100β, and RhoA in the prolonged compression group compared to the short compression group. The difference was statistically significant, indicating that earlier decompression can prevent the progress of secondary injuries due to higher expression levels of p75NTR, S100, and RhoA.

 This study demonstrated that early decompression of the spinal cord through the changes in p75NTR, S100β, and RhoA expression may modulate secondary injury events. Besides, it was found that using different inhibitors, especially for RhoA, might improve SCI-induced regeneration.