Spinal cord injury (SCI) can result in long-term loss of sensory and motor functions due to axon damage, gliosis, inflammation, and demyelination. Transected axons fail to regenerate in the adult mammalian CNS due to 1) lack of intrinsic regrowth ability, 2) inhibitory extrinsic cues including myelin associated proteins and chondroitin sulfate proteoglycans enriched in the glial scar as well as axon guidance molecules and 3) a physical gap of neural tissue for axon growth. Astrocytes constitute one of the principal components of the glial scar. In response to SCI, astrocytes become reactivated and start proliferation. How astrocyte reactivation is initiated and what cellular signaling pathways are involved in astrocyte polarization is largely unknown. Therefore, we hypothesize that Wnt/PCP signaling may be an important regulator of polarization of the reactive astrocytes after spinal cord injury, which may be important for glial scar formation and glial bridge formation.
Spinal cord injury (SCI) can result in long-term loss of sensory and motor functions due to axon damage, gliosis, inflammation, and demyelination. Astrocytes constitute one of the principal components of the glial scar. We propose to test the hypothesis that Wnt/PCP signaling may be an important regulator of polarization of the reactive astrocytes after spinal cord injury, which may be important for glial scar formation and glial bridge formation.
