Myelin abnormalities without oligodendrocyte loss in periventricular leukomalacia
Myelin abnormalities without oligodendrocyte loss in periventricular leukomalacia
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DOI：
10.1111/j.1750-3639.2007.00107.x
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发表时间：
2008-04-01
期刊：
影响因子：
6.4
通讯作者：
Kinney, Hannah C.
中科院分区：
文献类型：
--
作者：
Billiards, Saraid S.;Haynes, Robin L.;Kinney, Hannah C.
脑室周围白质软化症（PVL）长期幸存者经神经影像学检测到的髓鞘缺失的细胞基础了解甚少。我们检验了一个假设，即PVL中少突胶质细胞谱系（OL）细胞密度降低，从而导致后续的髓鞘缺失。我们使用基于计算机的方法，测定了18例PVL和18例年龄匹配的对照病例切片中用少突胶质细胞谱系标记物Olig2免疫染色的OL细胞密度。用髓鞘碱性蛋白（MBP）免疫染色评估髓鞘形成情况。我们发现PVL和对照病例在脑室周围或脑回内白质的Olig2细胞密度方面没有显著差异。然而，我们确实发现，与远处区域相比，坏死灶处的Olig2细胞密度显著增加。尽管在MBP免疫染色程度上没有发现显著差异，但我们观察到PVL的弥漫性和坏死性成分中MBP免疫染色存在质的异常。尽管Olig2细胞密度保持不变，但PVL中MBP免疫染色异常可能是由于少突胶质细胞成熟受阻、少突胶质细胞突起受损和/或轴突 - 少突胶质细胞信号传导受损所致。少突胶质细胞可能向损伤“核心”迁移以补充少突胶质细胞数量。这项研究为PVL幸存者中观察到的髓鞘缺失的细胞基础提供了新的见解。
The cellular basis of myelin deficits detected by neuroimaging in long-term survivors of periventricular leukomalacia (PVL) is poorly understood. We tested the hypothesis that oligodendrocyte lineage (OL) cell density is reduced in PVL, thereby contributing to subsequent myelin deficits. Using computer-based methods, we determined OL cell density in sections from 18 PVL and 18 age-adjusted control cases, immunostained with the OL-lineage marker Olig2. Myelination was assessed with myelin basic protein (MBP) immunostaining. We found no significant difference between PVL and control cases in Olig2 cell density in the periventricular or intragyral white matter. We did find, however, a significant increase in Olig2 cell density at the necrotic foci, compared with distant areas. Although no significant difference was found in the degree of MBP immunostaining, we observed qualitative abnormalities of MBP immunostaining in both the diffuse and necrotic components of PVL. Abnormal MBP immunostaining in PVL despite preserved Olig2 cell density may be secondary to arrested OL maturation, damage to OL processes, and/or impaired axonal-OL signaling. OL migration toward the "core" of injury may occur to replenish OL cell number. This study provides new insight into the cellular basis of the myelin deficits observed in survivors of PVL.