SPINAL-CORD MULTIPLE-SCLEROSIS LESIONS IN JAPANESE PATIENTS - SCHWANN-CELL REMYELINATION OCCURS IN AREAS THAT LACK GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP)
SPINAL-CORD MULTIPLE-SCLEROSIS LESIONS IN JAPANESE PATIENTS - SCHWANN-CELL REMYELINATION OCCURS IN AREAS THAT LACK GLIAL FIBRILLARY ACIDIC PROTEIN (GFAP)
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DOI：
10.1007/bf00687001
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发表时间：
1985-01-01
影响因子：
12.7
通讯作者：
WEBSTER, HD
中科院分区：
文献类型：
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作者：
ITOYAMA, Y;OHNISHI, A;WEBSTER, HD
为进一步研究多发性硬化（MS）损伤中许旺细胞髓鞘再生的作用，对8例日本MS患者的脊髓切片进行了Po糖蛋白（P0糖蛋白）、髓鞘碱性蛋白（MBP）和胶质细胞酸性蛋白（GFAP）的免疫组化染色。8例日本MS患者中有6例的脊髓切片含有大量具有抗Po免疫反应性的外周髓鞘。在6例患者中的4例中发现的病变中，存在数千个Po染色的PNS髓鞘。这些病变中坏死明显，包括一半以上的脊髓横截面积。外周来源的再生髓鞘的数量和密度远大于在白色[高加索]人的MS脊髓病变中观察到的。抗GFAP免疫反应存在于大多数脑和脊髓病变。然而，包含大量PNS髓鞘的病变区域缺乏抗GFAP免疫反应性。显然，大的、严重脱髓鞘和部分坏死的脊髓MS病变可能含有抑制纤维性星形胶质细胞增生的因子。这些因素，其他物质在大的病变和/或缺乏星形胶质细胞瘢痕，然后可以促进雪旺细胞的侵袭，增殖和髓鞘再生的幸存轴突。
To extend earlier observations on Schwann cell remyelination in multiple sclerosis (MS) lesions, Spinal cord sections from 8 Japanase MS patients were immunostained with antiserum to Po glycoprotein, a major constituent of peripheral nervous system (PNS) myelin, myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). Spinal cord sections from 6 of the 8 Japanese MS patients contained large clusters of peripheral myelin sheaths with anti-Po immunoreactivity. In lesions found in 4 of the 6 patients, thousands of Po-stained PNS myelin sheaths were present. Necrosis was prominent in these lesions which included more than half of the spinal cord''s transverse area. The number and density of regenerating myelin sheaths of peripheral origin were much greater than observed in MS spinal cord lesions of white [Caucasian] people. Anti-GFAP immunoreactivity was present in most brain and spinal cord lesions. However, the areas in lesions that contained large groups of PNS myelin sheaths lacked anti-GFAP immunoreactivty. Apparently, spinal MS lesions that are large, severely demyelinated and partially necrotic may contain factors that inhibit fibrous astrogliosis. These factors, other substances in the large lesions and/or the lack of astrocytic scarring could then promote Schwann cell invasion, multiplication and remyelination of surviving axons.