SCHWANN-CELLS DEGRADE MYELIN AND PROLIFERATE IN THE ABSENCE OF MACROPHAGES - EVIDENCE FROM IN-VITRO STUDIES OF WALLERIAN DEGENERATION
SCHWANN-CELLS DEGRADE MYELIN AND PROLIFERATE IN THE ABSENCE OF MACROPHAGES - EVIDENCE FROM IN-VITRO STUDIES OF WALLERIAN DEGENERATION
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DOI：
10.1007/bf01179817
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发表时间：
1995-09-01
期刊：
影响因子：
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通讯作者：
BUNGE, MB
中科院分区：
文献类型：
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作者：
FERNANDEZVALLE, C;BUNGE, RP;BUNGE, MB
周围神经干轴突连续性的中断会导致轴突和髓鞘的破坏，并移至损伤部位的远端，这一过程被称为沃勒变性。轴突和髓鞘碎片的清除归因于两种细胞类型的协同作用，即本土雪旺细胞和募集到组织损伤区域的巨噬细胞。最近在这一领域的研究表明，雪旺细胞在髓鞘降解中的作用有限，并强调了巨噬细胞的作用，不仅在清除髓鞘方面，而且在刺激雪旺细胞增殖方面也是如此，后者也发生在沃勒变性过程中。在这份报告中，我们证明了大鼠雪旺细胞能够在没有巨噬细胞的帮助下降解大量的髓鞘。从正常髓鞘大鼠背根神经节Newon/Schwann细胞共培养中摘除神经元胞体后进行观察。用相差显微镜、苏丹黑染色或电子显微镜观察髓鞘破坏的不同阶段。单个髓鞘节间破坏的时间进程在伤后2~10天不等，并在一定程度上取决于原始的节间长度。此外，我们还发现，在没有巨噬细胞的情况下，大多数参与沃勒变性的雪旺细胞在髓鞘降解成颗粒后进行细胞分裂，光镜下可见。通过对OX42、ED2和ED1巨噬细胞标志物的免疫染色评估，所使用的共培养基本上不含巨噬细胞。光镜和电子显微镜下未见巨噬细胞出现在已鉴定的雪旺细胞附近，此外，经荧光标记的乙酰化低密度脂蛋白标记，在未损伤的共培养中很少观察到巨噬细胞/单核细胞。这些结果支持了雪旺细胞在体外瓦勒变性过程中能够在没有巨噬细胞帮助的情况下进行短髓鞘片段的降解和增殖的能力。
Interruption of axonal continuity in peripheral nerve trunks leads to axonal and myelin breakdown and removal distal to the injury site, a process known as Wallerian degeneration. Clearance of axonal and myelin debris has been attributed to the cooperative actions of two cell types, the indigenous Schwann cells and macrophages recruited to the regions of tissue damage. Recent work in this area has suggested a limited role for Schwann cells in myelin degradation and has emphasized the role of macrophages, not only in myelin clearance but also in the stimulation of Schwann cell proliferation which also occurs during Wallerian degeneration. In this report, we demonstrate that rat Schwann cells are capable of substantial myelin degradation unaided by macrophages. Observations were made following excision of neuronal somata from well-myelinated rat dorsal root ganglion newon/Schwann cell co-cultures. The various stages of myelin breakdown were observed by phase microscopy, Sudan black staining or electron microscopy. The time course for breakdown of individual myelin internodes varied from 2 to 10 days after injury and was to some extent dependent upon the original intemodal length. Additionally, we show that most Schwann cells involved in Wallerian degeneration in the absence of macrophages undergo cell division following degradation of myelin into granules visible by light microscopy. The co-cultures employed were essentially free of macrophages as assessed by immunostaining for the OX42, ED2, and ED1 macrophage markers. No macrophages were detected by light or electron microscopy in the vicinity of the identified Schwann cells and furthermore, macrophages/monocytes were rarely observed in uninjured co-cultures as assessed by fluorochrome-conjugated acetylated LDL labelling. These results provide evidence in support of the ability of Schwann cells to carry out degradation of short myelin segments and to proliferate without macrophage assistance during Wallerian degeneration in vitro.