Ankerhold R, Leppert C A, Bastmeyer M, Stuermer C A
Division of Biology, University of Konstanz, Germany.
Glia. 1998 Jul;23(3):257-70.
The properties of glial cells in lesioned nerves contribute quite substantially to success or failure of axon regeneration in the CNS. Goldfish retinal axons regenerate after optic nerve lesion (ONS) and express the L1-like cell adhesion protein E587 antigen on their surfaces. Goldfish oligodendrocytes in vitro also produce E587 antigen and promote growth of both fish and rat retinal axons. To determine whether glial cells in vivo synthesize E587 antigen, in situ hybridizations with E587 antisense cRNA probes and light- and electron microscopic E587 immunostainings were carried out. After lesion, the goldfish optic nerve/tract contained glial cells expressing E587 mRNA, which were few in number at 6 days after ONS, increased over the following week and declined in number thereafter. Also, E587-immunopositive elongated cells with ultrastructural characteristics of oligodendrocytes were found. Thus, glial cells synthesize E587 antigen in spatiotemporal correlation with retinal axon regeneration. To determine the functional contribution of E587 antigen, axon-oligodendrocyte interactions were monitored in co-culture assays in the presence of Fab fragments of a polyclonal E587 antiserum. E587 Fabs in axon-glia co-cultures prevented the normal tight adhesion of goldfish retinal growth cones to oligodendrocytes and blocked the preferential growth of fish and rat retinal axons on the oligodendrocyte surfaces. The ability of glia in the goldfish visual pathway to upregulate the expression of E587 antigen and the growth supportive effect of oligodendrocyte-associated E587 antigen in vitro suggests that this L1-like adhesion protein promotes retinal axon regeneration in the goldfish CNS.
受损神经中胶质细胞的特性对中枢神经系统轴突再生的成败起着相当重要的作用。金鱼视网膜轴突在视神经损伤（ONS）后能够再生，并在其表面表达L1样细胞粘附蛋白E587抗原。体外培养的金鱼少突胶质细胞也能产生E587抗原，并促进金鱼和大鼠视网膜轴突的生长。为了确定体内胶质细胞是否合成E587抗原，进行了E587反义cRNA探针的原位杂交以及光镜和电镜下的E587免疫染色。损伤后，金鱼视神经/视束中含有表达E587 mRNA的胶质细胞，在视神经损伤后6天时数量较少，在接下来的一周内增加，此后数量下降。此外，还发现了具有少突胶质细胞超微结构特征的E587免疫阳性伸长细胞。因此，胶质细胞与视网膜轴突再生在时空上相关地合成E587抗原。为了确定E587抗原的功能作用，在多克隆E587抗血清的Fab片段存在的情况下，在共培养试验中监测轴突与少突胶质细胞的相互作用。轴突与胶质细胞共培养中的E587 Fabs阻止了金鱼视网膜生长锥与少突胶质细胞的正常紧密粘附，并阻断了金鱼和大鼠视网膜轴突在少突胶质细胞表面的优先生长。金鱼视觉通路中胶质细胞上调E587抗原表达的能力以及体外少突胶质细胞相关E587抗原的生长支持作用表明，这种L1样粘附蛋白促进了金鱼中枢神经系统中视网膜轴突的再生。
