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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Sialidase enhances spinal axon outgrowth in vivo
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Sialidase enhances spinal axon outgrowth in vivo

机译：唾液酸酶可增强体内的脊髓轴突生长

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摘要

The adult CNS is an inhibitory environment for axon outgrowth, severely limiting recovery from traumatic injury. This limitation is due, in part, to endogenous axon regeneration inhibitors (ARIs) that accumulate at CNS injury sites. ARIs include myelin-associated glycoprotein, Nogo, oligodendrocyte-myelin glycoprotein, and chondroitin sulfate proteoglycans (CSPGs). Some ARIs bind to specific receptors on the axon growth cone to halt outgrowth. Reversing or blocking the actions of ARIs may promote recovery after CNS injury. We report that treatment with sialidase, an enzyme that cleaves one class of axonal receptors for myelin-associated glycoprotein, enhances spinal axon outgrowth into implanted peripheral nerve grafts in a rat model of brachial plexus avulsion, a traumatic injury in which nerve roots are torn from the spinal cord. Repair using peripheral nerve grafts is a promising restorative surgical treatment in humans, although functional improvement remains limited. To model brachial plexus avulsion in the rat, C8 nerve roots were cut flush to the spinal cord and a peroneal nerve graft was inserted into the lateral spinal cord at the lesion site. Infusion of Clostridium perfringens sialidase to the injury site markedly increased the number of spinal axons that grew into the graft (2.6-fold). Chondroitinase ABC, an enzyme that cleaves a different ARI (CSPGs), also enhanced axon outgrowth in this model. in contrast, phosphatidylinositol-specific phospholipase C, which cleaves oligodendrocyte-myelin glycoprotein and Nogo receptors, was without benefit. Molecular therapies targeting sialoglycoconjugates and CSPGs may aid functional recovery after brachial plexus avulsion or other nervous system injuries and diseases.
机译：成人中枢神经系统是轴突生长的抑制环境，严重限制了创伤的恢复。该限制部分归因于积累在CNS损伤部位的内源性轴突再生抑制剂（ARIs）。 ARI包括髓磷脂相关糖蛋白，Nogo，少突胶质细胞髓磷脂糖蛋白和硫酸软骨素蛋白聚糖（CSPG）。一些ARIs结合到轴突生长锥上的特定受体上，以阻止生长。逆转或阻断ARI的作用可能会促进中枢神经系统损伤后的恢复。我们报道了唾液酸酶的治疗，该酶可裂解一类髓鞘相关糖蛋白的轴突受体，在臂丛神经撕脱的大鼠模型中，脊髓轴突的生长增强到植入的周围神经移植物中，这是一种创伤性损伤，其中神经根从脊髓。尽管功能改善仍然有限，但使用外周神经移植物修复是人类有希望的修复性手术治疗。为了模拟大鼠臂丛神经撕脱，将C8神经根切成与脊髓齐平，并在病变部位将腓神经移植物插入到脊髓外侧。将产气荚膜梭菌唾液酸酶注入损伤部位显着增加了生长到移植物中的脊髓轴突的数量（2.6倍）。软骨素酶ABC（一种裂解不同ARI（CSPG）的酶）在该模型中也增强了轴突的生长。相反，切割少突胶质细胞-髓磷脂糖蛋白和Nogo受体的磷脂酰肌醇特异性磷脂酶C是没有益处的。靶向唾液酸糖缀合物和CSPG的分子疗法可有助于臂丛神经撕脱或其他神经系统损伤和疾病后的功能恢复。

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