Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage
Astrocytic Demise in the Developing Rat and Human Brain after Hypoxic-Ischemic Damage
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DOI：
10.1159/000232564
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发表时间：
2009-01-01
影响因子：
2.9
通讯作者：
Charriaut-Marlangue, Christiane
中科院分区：
文献类型：
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作者：
Gelot, Antoinette;Villapol, S.;Charriaut-Marlangue, Christiane
为了探讨未成熟脑对缺氧缺血（HI）的选择性易感性的生理病理学机制，我们比较了出生后7天大鼠使用新生儿中风模型与人胎儿和新生儿脑中发生的损伤。我们首先观察到，灰质和白色病变表现出相似的组织（核心与细胞损失和/或空腔和半影）和实验和人类HI病变之间的进化模式。然后，我们观察到，在中间的白色物质，GFAP和波形蛋白阳性星形胶质细胞表现出clamatodendrosis，并代表了一个主要的细胞群体参与细胞死亡在人脑（56.3和67.9%，分别）。在大鼠脑中，GFAP和TUNEL阳性星形胶质细胞也非常脆弱，在缺血后6（31%）和72（58%）小时之间增加。总之，这些结果表明，星形胶质细胞功能障碍可能在决定急性缺氧缺血性损伤的进展和结果中起着关键作用，特别是在发育中的大脑中。版权所有（C）2009 S. Karger AG，巴塞尔
In order to approach the physiopathological mechanism underlying the selective susceptibility of the immature brain to hypoxia-ischemia (HI), we have compared the lesions experimentally induced in postnatal day 7 rats using a model of neonatal stroke with those occurring in human fetal and neonatal brains. We first observed that gray and white matter lesions demonstrated a similar organization (core with cell loss and/or cavity and penumbra) and evolutionary pattern between experimental and human HI lesions. We then observed that, in the intermediate white matter, GFAP- and vimentin-positive astrocytes exhibited clasmatodendrosis and represent a major cell population involved in cell death in human brains (56.3 and 67.9%, respectively). In rat brains, GFAP- and TUNEL-positive astrocytes were also highly vulnerable, increasing between 6 (31%) and 72 (58%) hours after ischemia. Together, these results indicate that astroglial dysfunction may play a critical role in determining the progress and outcome of acute hypoxic-ischemic injury particularly in the developing brain. Copyright (C) 2009 S. Karger AG, Basel