Signaling mechanisms for astrocyte polarization during glial scar formation after spinal cord injury

脊髓损伤(SCI)可由于轴突损伤而导致长期的感觉和运动功能丧失， 胶质增多症、炎症和脱髓鞘。成年哺乳动物中枢神经系统内横断轴突不能再生 1)缺乏内在再生能力，2)抑制外在信号，包括髓鞘相关蛋白和 硫酸软骨素蛋白多糖在胶质瘢痕和轴突引导分子中丰富，3)a 神经组织为轴突生长提供的物理间隙。星形胶质细胞是胶质瘢痕的主要成分之一。作为对脊髓损伤的反应，星形胶质细胞重新激活并开始增殖。星形胶质细胞的重新激活是如何启动的，以及哪些细胞信号通路参与了星形胶质细胞的极化，这在很大程度上是未知的。因此，我们推测Wnt/PCP信号可能是脊髓损伤后反应性星形胶质细胞极化的重要调节因子，可能在胶质瘢痕形成和胶质桥形成中起重要作用。

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.