Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid
Increased neuronal and astroglial aquaporin-1 immunoreactivity in rat striatum by chemical preconditioning with 3-nitropropionic acid
复制标题
3-硝基丙酸化学预处理增加大鼠纹状体神经元和星形胶质细胞水通道蛋白-1 的免疫反应性
DOI：
10.1016/j.neulet.2016.05.021
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Yoshikazu Ugawa
中科院分区：
文献类型：
--
作者：
Akihiko Hoshi;Ayako Tsunoda;Teiji Yamamoto;Mari Tada;Akiyoshi Kakita;Yoshikazu Ugawa
水通道蛋白-1（AQP 1）是一种在脉络丛中表达的水通道，参与脑脊液的形成。有趣的是，在某些病理条件下，反应性星形胶质细胞也在中枢神经系统中表达AQP 1。另一方面，3-硝基丙酸（3-nitropropionic acid，3 NP）是一种线粒体毒素，可导致纹状体选择性变性;然而，其化学预处理对脑缺血具有神经保护作用。我们先前报道，轻度应用3 NP伴随着许多反应性星形胶质细胞在大鼠纹状体没有典型的坏死病变。因此，我们研究是否AQP 1在大鼠纹状体可以上调反应性星形胶质细胞增生使用3 NP模型。免疫组织化学或免疫荧光分析表明，反应性星形胶质细胞在纹状体，上调胶质细胞酸性蛋白和谷氨酰胺合成酶，诱导温和剂量的3 NP管理。有趣的是，3 NP处理后，AQP 1不仅在星形胶质细胞亚群中强烈表达，而且在神经元中也强烈表达。AQP 1免疫反应在亚毒性早期（ES：24-48 h）增强，而在延迟亚毒性期（DS：96-120 h）减弱。相反，AQP 4在纹状体的表达下调后，3 NP治疗，特别是在ES阶段。在亚毒性3 NP处理下诱导的AQP 1上调/AQP 4下调可能在纹状体的水稳态和细胞活力中起关键作用。
Aquaporin-1 (AQP1) is a water channel expressed in the choroid plexus and participates in forming cerebrospinal fluid. Interestingly, reactive astrocytes also express AQP1 in the central nervous system under some pathological conditions. On the other hand, 3-nitropropionic acid (3NP) is a mitochondrial toxin that causes selective degeneration of striatum; however, its chemical preconditioning is neuroprotective against cerebral ischemia. We previously reported that mild 3NP application is accompanied with numerous reactive astrocytes in rat striatum devoid of typical necrotic lesions. Therefore, we studied whether AQP1 in the rat striatum could be upregulated with reactive astrocytosis using the 3NP model. Immunohistochemical or immunofluorescence analysis showed that reactive astrocytosis in the striatum, which upregulates glial fibrillary acidic protein and glutamine synthetase, was induced by mild doses of 3NP administration. Intriguingly, after 3NP treatment, AQP1 was intensely expressed not only by the subpopulation of astroglia but also by neurons. The AQP1 immunoreactivity became more intensified at the early-subtoxic stage (ES: 24–48 h), but not as much in the delayed-subtoxic stage (DS: 96–120 h). In contrast, AQP4 expression in the striatum was downregulated after 3NP treatment, in particular during the ES stage. AQP1 upregulation/AQP4 downregulation induced under subtoxic 3NP treatment may play a pivotal role in water homeostasis and cell viability in the striatum.