Schwannosis: Role of gliosis and proteoglycan in human spinal cord injury
Schwannosis: Role of gliosis and proteoglycan in human spinal cord injury
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DOI：
10.1089/neu.2000.17.781
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发表时间：
2000-09-01
影响因子：
4.2
通讯作者：
Dietrich, D
中科院分区：
文献类型：
--
作者：
Bruce, JH;Norenberg, MD;Dietrich, D
脊髓损伤（SCI）后出现雪旺病（雪旺细胞和神经纤维的异常增殖）。在这项研究中，我们研究了人类脊髓损伤后神经鞘病的发病率，并探讨了其与神经胶质瘤的关系。我们发现65例人类脊髓损伤患者中有32例（48%）在损伤后24小时至24年存活；在存活超过4个月的患者中，这一发生率上升至82%。在受伤后存活少于4个月的病例中未观察到雪旺氏症。在受影响的病例中，通常在神经胶质纤维酸性蛋白（GFAP）免疫反应性较低的区域发现，这表明神经胶质增生减少可能导致脊髓损伤后雪旺细胞的异常增殖。由于硫酸软骨素蛋白多糖（CSPG）被认为在雪旺细胞/神经胶质相互作用中起作用，我们对CSPG进行了免疫组织化学染色，以研究其与雪旺病的潜在关系。损伤脐带的CSPG通常与血管壁有关，但有时也见于反应性星形胶质细胞。脊髓损伤合并雪旺病时，CSPG染色更为明显，且主要局限于增殖的雪旺细胞的细胞外基质和基层。我们的研究表明，许旺细胞可能已经从脊髓根移位，并通过脊髓表面的断裂引入损伤的脊髓，能够增殖并产生CSPG，特别是在胶质细胞增生减少的情况下。由于CSPG与神经突生长的抑制有关，异常雪旺细胞增加CSPG的产生可能会损害脊髓损伤后的再生。
Schwannosis (aberrant proliferation of Schwann cells and nerve fibers) has been reported following spinal cord injury (SCI). In this study, we examined the incidence of schwannosis following human SCI, and investigated its relationship to gliosis. We found evidence of schwannosis in 32 out of 65 cases (48%) of human SCI that survived 24 h to 24 years after injury; this incidence rose to 82% in those patients who survived for more than 4 months. Schwannosis was not observed in cases that survived less than 4 months after injury. In affected cases, it was generally noted in areas that had low immunoreactivity for glial fibrillary acidic protein (GFAP), suggesting that reduced gliosis might have contributed to the aberrant proliferation of Schwann cells following SCI. Since chondroitin sulfate proteoglycan (CSPG) has been proposed to play a role in Schwann cell/glial interaction, we performed immunohistochemical staining for CSPG to investigate its potential relationship with schwannosis. CSPG in the injured cord was generally associated with the blood vessel walls, but was also sometimes noted in reactive astrocytes. In SCI with schwannosis, CSPG staining was more prominent and confined largely to the extracellular matrix and basal lamina of proliferating Schwann cells. Our study suggests that Schwann cells, which may have been displaced from spinal roots and introduced into the injured cord through a break in the pial surface, are capable of proliferating and producing CSPG, particularly in the setting of reduced gliosis. Since CSPG has been associated with inhibition of neurite outgrowth, its increased production by aberrant Schwann cells may impair spinal cord regeneration after injury.