RXRα Blocks Nerve Regeneration after Spinal Cord Injury by Targeting p66shc

Figure 1

RXRα inhibited nerve regeneration after spinal cord injury. (a) β-III-Tubulin immunohistochemical staining showed that after spinal cord injury, the number of neuronal cells in the injured area was reduced, and the neurite continuity was interrupted. After RXRα agonist administration, the morphology of the tissue lacked integrity, and the neurons were in an apoptotic state; there were no continuous neurites. After RXRα antagonist administration, the number of neuronal cells increased, the cell morphology was good, and there was some neurite regeneration. (b) β-III-Tubulin immunofluorescence staining of primary spinal cord neuronal cells cultured in vitro showed that after scratch damage, the length of neurites in the RXRα agonist group was significantly shorter than that of neurites in the control group, while the length of neurites in the RXRα antagonist group was significantly longer than that of neurites in the control group. The results suggest that RXRα inhibits neurite regeneration after spinal cord injury. (c) Compared with that of neurites in the postinjury control group, the length of the regenerated neurites in the spinal cord slices cultured in vitro in the RXRα agonist group was significantly shortened after injury, while the length of the regenerated neurites in the RXRα antagonist group significantly increased. The length of postinjury neurites in each group was significantly shorter than that before injury. /group; vs. control, , scale bar: 50 or 100 μm.

(a)

(b)

(c)