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感觉和运动功能的长期丧失， 神经胶质增生、炎症和脱髓鞘。成年哺乳动物中枢神经系统中横断的轴突不能再生， 1）缺乏内在的再生能力，2）抑制性的外部线索，包括髓鞘相关蛋白， 在神经胶质瘢痕中富集的硫酸软骨素蛋白聚糖以及轴突导向分子，和3）a 轴突生长的神经组织的物理间隙。星形胶质细胞构成神经胶质瘢痕的主要成分之一。作为对SCI的响应，星形胶质细胞被重新激活并开始增殖。星形胶质细胞的活化是如何启动的，以及星形胶质细胞极化中涉及哪些细胞信号通路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，这可能对胶质瘢痕形成和胶质桥形成很重要。

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.