Shearer M C, Fawcett J W
Department of Physiology, University of Cambridge, England.
Cell Tissue Res. 2001 Aug;305(2):267-73. doi: 10.1007/s004410100384.
Following injuries to the adult mammalian CNS meningeal cells migrate into the lesion cavity, forming a fibrotic scar and accessory glia limitans. This infiltration re-establishes the meningeal layer that normally surrounds the CNS, and so reforms the barrier between the CNS and external environment, thus protecting the damaged region from events outside it. However, the newly formed meningeal layer and glia limitans may impede subsequent nerve regeneration through the injured region. This structure can be modelled in vitro using an astrocyte/meningeal co-culture system. We have examined patterns of neurite outgrowth on such cultures, and we find that axons cross readily from meningeal cells to astrocytes, but are unwilling to cross in the other direction. The distribution of cell surface and matrix molecules on these cultures is described, and the effect of various pharmacological interventions which can affect axon growth between the two cell types is summarised in this review.
成年哺乳动物中枢神经系统（CNS）受伤后，脑膜细胞会迁移至损伤腔，形成纤维化瘢痕和附属胶质界膜。这种浸润重新建立了通常环绕中枢神经系统的脑膜层，从而重新形成中枢神经系统与外部环境之间的屏障，进而保护受损区域免受外部事件的影响。然而，新形成的脑膜层和胶质界膜可能会阻碍随后的神经通过损伤区域再生。这种结构可以在体外使用星形胶质细胞/脑膜共培养系统进行模拟。我们已经研究了此类培养物上神经突生长的模式，并且发现轴突很容易从脑膜细胞延伸至星形胶质细胞，但不愿朝相反方向延伸。本文综述了这些培养物上细胞表面和基质分子的分布情况，以及各种能够影响两种细胞类型之间轴突生长的药理学干预措施的作用。
