Chen Zhi Jiang, Ughrin Yvonne, Levine Joel M
Department of Neurobiology and Behavior, SUNY at Stony Brook, New York 11794, USA.
Mol Cell Neurosci. 2002 May;20(1):125-39. doi: 10.1006/mcne.2002.1102.
The glial scar that forms at the site of injury is thought to be a biochemical and physical barrier to successful regeneration, although the molecules responsible for this barrier function are not well understood. Glia scars contain large numbers of oligodendrocyte precursor cells (OPCs) and these cells can produce several different growth-inhibitory chondroitin sulfate proteoglycans (CSPGs), including NG2, neurocan, and phosphacan. Here, we used membrane-based assays to show that the surface of OPCs is both nonpermissive and inhibitory for neurite outgrowth. Inhibition of growth by OPC is reversed by treatment with antibodies against the NG2 CSPG and the expression of NG2 is sufficient to change a growth-permissive cell surface to a nonpermissive surface. These result suggest that the OPCs that accumulate rapidly at sites of CNS injury can contribute to the creation of an environment that inhibits nerve regeneration and that NG2 is a necessary feature of that environment.
损伤部位形成的胶质瘢痕被认为是成功再生的生化和物理屏障,尽管负责这种屏障功能的分子尚未完全明确。胶质瘢痕包含大量少突胶质前体细胞(OPCs),这些细胞可产生几种不同的生长抑制性硫酸软骨素蛋白聚糖(CSPGs),包括NG2、神经蛋白聚糖和磷蛋白聚糖。在此,我们使用基于膜的分析方法表明,OPCs的表面对神经突生长既不允许也具有抑制作用。用抗NG2 CSPG的抗体处理可逆转OPC对生长的抑制作用,且NG2的表达足以将允许生长的细胞表面转变为不允许生长的表面。这些结果表明,在中枢神经系统损伤部位迅速聚集的OPCs可能有助于营造抑制神经再生的环境,且NG2是该环境的一个必要特征。