Multiple sclerosis: Death receptor expression and oligodendrocyte apoptosis in established lesions
Multiple sclerosis: Death receptor expression and oligodendrocyte apoptosis in established lesions
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DOI：
10.1016/j.jneuroim.2007.05.018
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发表时间：
2007-08-01
影响因子：
3.3
通讯作者：
Raine, Cedric S.
中科院分区：
文献类型：
--
作者：
Cannella, Barbara;Gaupp, Stefanie;Raine, Cedric S.
为了确定TNF和TRAIL死亡受体（DR）和诱饵受体（DcR）是否在慢性多发性硬化（NIS）病变中的少突胶质细胞耗竭中发挥作用，我们研究了NIS和nonNIS脑组织中少突胶质细胞和体外人少突胶质细胞上这些分子的存在和功能。为此，我们进行了免疫细胞化学，蛋白质印迹，TUNEL和流式细胞术分析DR和细胞凋亡的存在下，新鲜冷冻的CNS组织的部分慢性NIS的情况下，其他神经系统疾病和正常人，并在胎儿人少突胶质细胞在体外。结果表明，虽然少突胶质细胞表现出DR和DcR，特别是在体外，有没有偏好的现象NIS和凋亡的少突胶质细胞，常见的培养后与TRAIL连接，是可以忽略不计的CNS组织原位。因此，在所有检测的人CNS样本中，少突胶质细胞凋亡死亡是罕见事件。我们推测，虽然少突胶质细胞凋亡可能占上风，在NIS的初始阶段，从我们的研究结果，其他机制可能占其损失在既定的病变和诱饵受体可能发挥保护作用，少突胶质细胞的生存。(c)2007 Elsevier B.V.保留所有权利。
To determine whether TNF and TRAIL death receptors (DR), and decoy receptors (DcR), play a role in oligodendrocyte depletion in the lesions of chronic multiple sclerosis (NIS), we investigated the presence and functionality of these molecules on oligodendrocytes in NIS and nonNIS brain tissue and on human oligodendrocytes in vitro. For this, we performed immunocytochemistry, Western blotting, TUNEL and FACS analysis for the presence of DR and apoptosis in sections of fresh frozen CNS tissue from cases of chronic NIS, other neurologic diseases and normals, and in fetal human oligodendrocytes in vitro. The results showed that although oligodendrocytes demonstrated both DR and DcR, particularly in vitro, there was no predilection of the phenomenon for NIS and apoptosis of oligodendrocytes, common in cultures after ligation with TRAIL, was negligible in CNS tissue in situ. Thus, death of oligodendrocytes by apoptosis was an infrequent event in all human CNS samples examined. We postulate that while oligodendrocyte apoptosis might prevail during the initial stages of NIS, from our findings other mechanisms probably account for their loss in the established lesion and decoy receptors may play a protective role in oligodendrocyte survival. (c) 2007 Elsevier B.V. All rights reserved.