Fgf2 improves functional recovery—decreasing gliosis and increasing radial glia and neural progenitor cells after spinal cord injury

A major impediment for recovery after spinal cord injury (SCI) is the glial scar formed by proliferating reactive astrocytes. The researchers aimed to find factors that may reduce glial scarring, increase neuronal survival, and promote neurite outgrowth to improve outcomes after SCI. The study found that Fgf2 treatment decreased inflammation, reduced monocyte/macrophage infiltration, and decreased gliosis. Fgf2 also induced astrocytes to adopt a polarized morphology and increased expression of radial markers, suggesting a shift toward a pro-regenerative state. Furthermore, Fgf2 treatment promotes the formation of parallel glial processes, termed 'bridges,' at the injury site, facilitating the regeneration of axons. Fgf2 also increased Sox2-expressing cells and neurogenesis at the lesion site, which correlated with enhanced functional recovery.

• 1
  Fgf2 treatment decreases the expression of TNF-α, reduces monocyte/macrophage infiltration, and decreases gliosis at the lesion site after spinal cord injury in mice.
• 2
  Fgf2 induces astrocytes to adopt a polarized morphology, increases the expression of radial markers like Pax6 and nestin, and decreases levels of CSPGs, creating a pro-regenerative environment.
• 3
  Fgf2 promotes the formation of parallel glial processes ('bridges') at the lesion site, enabling regenerating axons to traverse the injury, and increases Sox2-expressing cells and neurogenesis, leading to enhanced functional recovery.