Expression and activation of Ephexin is altered after spinal cord injury

Traumatic spinal cord injury (SCI) often results in failure of axon regeneration due to inhibitory molecular interactions. The activation of Eph signaling pathways can modulate growth cone dynamics and repulsion through ephexin, a guanine nucleotide exchange factor (GEF). This study investigates the expression profile of ephexin after SCI. The study found that ephexin expression increased in injured rats at 4 and 7 days post-injury but returned to normal levels by 14 days. However, phosphorylated ephexin (activated ephexin) was elevated from day 2 until 14 days post-injury. Ephexin was found in neurons, axons, microglia/macrophages, and reactive astrocytes and co-localized with EphA3, A4, and A7. The results demonstrate the presence of ephexin in the adult spinal cord and its activation after SCI, suggesting its role in the non-permissive environment after spinal cord injury.

• 1
  Ephexin protein expression increases after SCI, peaking at 4-7 days post-injury and returning to normal levels by 14 days.
• 2
  Phosphorylation of ephexin, indicating its activation, is significantly increased from 2 to 14 days post-injury.
• 3
  Ephexin co-localizes with EphA3, EphA4, and EphA7 receptors in neurons, axons, astrocytes, and microglia/macrophages in the injured spinal cord.