CHARACTERIZATION OF A NEURITE OUTGROWTH INHIBITOR EXPRESSED AFTER CNS INJURY
CHARACTERIZATION OF A NEURITE OUTGROWTH INHIBITOR EXPRESSED AFTER CNS INJURY
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DOI：
10.1111/j.1460-9568.1993.tb00512.x
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发表时间：
1993-05-01
影响因子：
3.4
通讯作者：
NIETOSAMPEDRO, M
中科院分区：
文献类型：
--
作者：
BOVOLENTA, P;WANDOSELL, F;NIETOSAMPEDRO, M
反应性神经胶质增生是对中枢神经系统灰质和白色物质损伤的普遍反应，是哺乳动物轴突再生的严重障碍。在培养中，来自正常大鼠脑组织的无髓鞘质膜促进了神经突的生长，而从损伤组织中纯化的无髓鞘膜则具有抑制作用。抑制活性能被去污剂增溶，对糖胺聚糖裂解酶敏感，在凝胶过滤层析中洗脱出的表观分子量为160-220 kDa。当以表面结合分子的形式存在时，抑制剂阻止神经突的起始;当以可溶性形式加入到生长的神经突中时，它诱导它们的收缩。这些结果提供了支持经典观点的细胞和分子证据，即在哺乳动物中枢神经系统中，损伤诱发的神经胶质增生与能够阻止神经突生长的分子的表达相关。
Reactive gliosis, a general response to injury in the central nervous system grey and white matter, represents a serious obstacle to axonal regeneration in.mammals. In culture, myelin-free plasma membranes from normal rat brain tissue promoted neurite outgrowth, whereas myelin-free membranes purified from injured tissue were inhibitory. The inhibitory activity could be solubilized by detergent, was sensible to glycosaminoglycan lyase digestion and eluted with an apparent molecular weight of 160-220 kDa in gel filtration chromatography. When presented as a surface-bound molecule, the inhibitor prevented neurite initiation; when added in a soluble form to growing neurites, it induced their retraction. These results provide cellular and molecular evidence supporting the classical view that, in the mammalian central nervous system, damage-evoked gliosis correlates with the expression of molecules capable of preventing neurite outgrowth.