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首页> 外文期刊>Neuropathology: official journal of the Japanese Society of Neuropathology >Decrease of aquaporin-4 and excitatory amino acid transporter-2 indicate astrocyte dysfunction for pathogenesis of cortical degeneration in HIV-associated neurocognitive disorders
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Decrease of aquaporin-4 and excitatory amino acid transporter-2 indicate astrocyte dysfunction for pathogenesis of cortical degeneration in HIV-associated neurocognitive disorders

机译：水素-4和兴奋性氨基酸转运蛋白-2的减少表明了艾滋病毒相关神经认知障碍中皮质变性的发病机制的星形胶质细胞功能障碍

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Human immunodeficiency virus (HIV) encephalitis and degeneration of cerebral cortex are established histopathologies of HIV-associated neurocognitive disorders (HAND). We previously reported decreased excitatory amino acid transporter-2 (EAAT-2) and astrocytic apoptosis in cortical degeneration using SIVmac239 and simian-human immunodeficiency virus (SHIV)-infected macaques and human AIDS autopsy cases. In the present study, we added highly pathogenic SIVsm543-3-infected macaques. These animals showed similar degenerative changes in the frontal cortex. Using 11 SIV-infected macaques, three SIVsm543-3, five SIVmac239 and three SHIV, we compared brain pathology caused by three different viruses and further analyzed the pathogenic process of HAND. We noticed vacuolar changes in perivascular processes of astrocytes by electron microscopy, and examined expression of astrocyte-specific protein aquaporin-4 (AQP4) by immunohistochemistry. APQ4 was diffusely positive in the neuropil and perivascular area in control brains. There was patchy or diffuse decrease of AQP4 staining in the neuropil of SIV-infected macaques, which was associated with EAAT-2 staining by double immunostaining. A quantitative analysis demonstrated significant positive correlation between areas of AQP4 and EAAT-2. Some astrocytes express EAAT-2 but not AQP4, and decrease of EAAT-2 expression tended to be less than the decrease of AQP4. Active-caspase-3 immunostaining demonstrated apoptosis of neurons and astrocytes in the area of AQP4/EAAT-2 reduction. These results suggest that AQP4 is damaged first and decrease of EAAT-2 may follow in pathogenesis of cortical degeneration. This is the first demonstration of decrease of AQP4 and its association with EAAT-2 decrease in AIDS brain, suggesting a role in the pathogenesis of HAND.
机译：人类免疫缺陷病毒（HIV）脑炎和脑皮层的退化是艾滋病毒相关神经认知障碍（手）的组织病理学。我们以前报道，使用SiVMac239和Simian-Lumalofice缺陷病毒（Shiv） - 肌肉尸检病例，在皮质变性中报告了兴奋性氨基酸转运蛋白-2（EAAT-2）和星形胶质细胞凋亡。在本研究中，我们添加了高致病性Sivsm543-3感染的猕猴。这些动物在额叶中显示出类似的退行性变化。使用11个SIV感染的猕猴，三个SIVSM543-3，五个SIVMAC239和三种SHIV，我们比较了三种不同病毒引起的脑病理，并进一步分析了手的致病过程。我们注意到电子显微镜的星形胶质细胞的血管内过程的真空变化，并通过免疫组化检查了星形胶质细胞特异性蛋白质水上蛋白-4（AQP4）的表达。 APQ4在对照大脑中神经疏松和血管外区域漫反射。 SIV感染的猕猴的神经尿嘧啶中AQP4染色的斑食或弥漫性降低，其通过双免疫染色与EAAT-2染色相关。定量分析表现出AQP4和EAAT-2的区域之间的显着正相关。一些星形胶质细胞表达EAAT-2但不是AQP4，并且EAAT-2表达的减少趋于小于AQP4的降低。活性Caspase-3免疫染色在AQP4 / EAAT-2的降低区域中显示了神经元和星形胶质细胞的凋亡。这些结果表明AQP4损坏，首先损坏，EAAT-2的减少可能遵循皮质变性的发病机制。这是AQP4降低的第一次证明及其与EAAT-2艾滋病大脑减少的关系，表明在手发病机制中的作用。

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