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难治性癫痫患者颞叶新皮质前部水通道蛋白-1表达增加。

Increased expression of aquaporin-1 in the anterior temporal neocortex of patients with intractable epilepsy.

作者信息

Zhou Shengnian, Sun Xian, Liu Liqing, Wang Xuefeng, Liu Kunbin

机构信息

Department of Neurology, Qilu Hospital, Jinan 250012, China.

出版信息

Neurol Res. 2008 May;30(4):400-5. doi: 10.1179/174313208X300431.

Abstract

OBJECTIVE

Aquaporin-1 (AQP1), the osmotic water channel, is located in choroidal plexus, which facilitates the cerebrospinal fluid formation in central nervous system (CNS). AQP1 has been speculated to maintain the homeostasis of intracellular and extracellular water in the brain, while the intractable epilepsy (IE) may be related to the imbalance in water and ion homeostasis.

METHODS

To investigate the role of AQP1 in pathophysiology of IE, we studied the expression of AQP1 in surgical samples of the anterior temporal neocortex of patients with IE and the age-matched controls samples.

RESULTS

Using immunohistochemistry, it was shown that AQP1 expression increased in astrocytes, but not in neurons or oligodendrocytes. Double-label immunofluorescence and confocal microscopy disclosed AQP1 immunoreactivity at the astrocyte membranes, where the most abundant expression was in the perivascular glial processes, which were recognized with antiglial fibrillary acidic protein antibodies (anti-GFAP).

CONCLUSION

For the first time, we showed high expression of AQP1 water channels in IE cases and suggest two mechanisms to explain this finding. Increased AQP1 expression of astrocytes may be a cause or a consequence of IE. Thus, additional works are needed to elucidate the true mechanism underlying their relationship.

摘要

目的

水通道蛋白1(AQP1)作为渗透水通道,位于脉络丛中,有助于中枢神经系统(CNS)中脑脊液的形成。据推测,AQP1可维持脑内细胞内和细胞外水的稳态,而难治性癫痫(IE)可能与水和离子稳态失衡有关。

方法

为研究AQP1在IE病理生理学中的作用,我们研究了IE患者颞叶新皮质手术样本及年龄匹配的对照样本中AQP1的表达情况。

结果

免疫组织化学结果显示,AQP1在星形胶质细胞中表达增加,但在神经元或少突胶质细胞中未增加。双重标记免疫荧光和共聚焦显微镜检查显示,AQP1免疫反应性存在于星形胶质细胞膜上,其中最丰富的表达位于血管周围的胶质突起中,这些突起可被抗胶质纤维酸性蛋白抗体(抗GFAP)识别。

结论

我们首次在IE病例中发现AQP1水通道高表达,并提出两种机制来解释这一发现。星形胶质细胞中AQP1表达增加可能是IE的原因或结果。因此,需要更多研究来阐明它们之间关系的真正机制。

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