Aquaporin-4 and brain edema.
Aquaporin-4 and brain edema.
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DOI：
10.1007/s00467-006-0411-0
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发表时间：
2007-06
期刊：
影响因子：
--
通讯作者：
Verkman AS
中科院分区：
文献类型：
--
作者：
Papadopoulos MC;Verkman AS
水通道蛋白4（AQP4）是一种在大脑中强烈表达的水通道蛋白，主要在脑实质与主要液体腔室（包括脑脊液和血液）之间边界的星形胶质细胞足突中表达。这种分布表明AQP4控制着进出脑实质的水通量。利用AQP4基因敲除小鼠进行的实验为AQP4参与脑水平衡提供了有力证据。AQP4基因敲除小鼠可免受水中毒、脑缺血或脑膜炎所导致的细胞性（细胞毒性）脑水肿的影响。然而，AQP4缺失会加重由肿瘤、皮质冷冻、脑实质内液体输注或脑脓肿所产生的血管源性（液体渗漏）脑水肿。在细胞毒性水肿中，AQP4缺失会减慢水进入大脑的速度，而在血管源性水肿中，AQP4缺失会降低水从脑实质流出的速度。AQP4缺失还会使梗阻性脑积水恶化。最近，还发现AQP4在与脑水肿无关的过程中发挥重要作用，包括星形胶质细胞迁移和神经元兴奋性。这些发现表明，调节AQP4的表达或功能可能对几种脑部疾病有益，包括低钠性脑水肿、脑积水、中风、肿瘤、感染、癫痫和创伤性脑损伤。
Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury.
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影响因子：
82.9
作者：
Manley, GT;Fujimura, M;Verkman, AS
通讯作者：
Verkman, AS
影响因子：
4.8
作者：
Papadopoulos, MC;Verkman, AS
通讯作者：
Verkman, AS
影响因子：
3.3
作者：
LEHMENKUHLER, A;SYKOVA, E;NICHOLSON, C
通讯作者：
NICHOLSON, C
影响因子：
10.4
作者：
RODIER, PM
通讯作者：
RODIER, PM
影响因子：
4.1
作者：
KIMELBERG, HK
通讯作者：
KIMELBERG, HK