Expression and localization of prostaglandin transporter in Alzheimer disease brains and age-matched controls
Expression and localization of prostaglandin transporter in Alzheimer disease brains and age-matched controls
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DOI：
10.1016/j.jneuroim.2008.01.014
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发表时间：
2008-03-01
影响因子：
3.3
通讯作者：
Dore, Sylvain
中科院分区：
文献类型：
--
作者：
Choi, Koyi;Zhuang, Hean;Dore, Sylvain
神经炎症是神经退行性疾病的主要贡献者，涉及活化的小胶质细胞、反应性星形胶质细胞和浸润性炎性细胞的贡献。压力和各种急性或慢性脑损伤刺激自由基和谷氨酸的产生，触发炎症途径，导致趋化因子，细胞因子和前列腺素的增加。前列腺素是炎症的脂质介质，由花生四烯酸通过环氧合酶产生。一般认为它们存在于所有组织和器官中。它们通过细胞膜/细胞器的脂质双层的转运由前列腺素转运蛋白（PGT）促进。在这项研究中，额中回脑组织诊断为阿尔茨海默病（AD）和年龄匹配的对照组的大脑，以确定PGT的蛋白质表达模式和其可能的作用，在调制与AD相关的神经炎症。免疫组织化学和免疫荧光研究表明，PGT蛋白表达在所有的脑组织检查，并定位于神经元，小胶质细胞和星形胶质细胞。有趣的是，蛋白质印迹分析显示，AD患者的PGT水平显著低于年龄匹配的对照组脑匀浆。进一步的工作是有必要的，以解决的可能性和影响，阿维兰丁可能不会在AD大脑中以适当的速度清除。(C)2008 Elsevier B. V.保留所有权利。
Neuroinflammation, a major contributor to neurodegenerative diseases, involves the contribution of activated microglia, reactive astrocytes, and infiltrating inflammatory cells. Stress and various acute or chronic brain injuries stimulate the generation of free radicals and glutamate, triggering inflammatory pathways that lead to increases in chemokines, cytokines, and Prostaglandins. Prostaglandins are lipid mediators of inflammation that are produced from arachidonic acid by cyclooxygenase enzymes. They are generally believed to be in all tissues and organs. Their transport through the lipid bilayers of the cell membranes/organelles is facilitated by the prostaglandin transporter (PGT). In this study, middle frontal gyrus brain tissue from patients diagnosed with Alzheimer disease (AD) and that of age-matched control brains were examined to determine the protein expression pattern of PGT and its possible role in modulating neuroinflammation associated with AD. Immunohistochemical and immunofluorescent studies showed that PGT protein was expressed in all the brain tissues examined and was localized in neurons, microglia, and astrocytes. Interestingly, Western blot analysis revealed that the PGT level was significantly less in AD than in age-matched control brain homogenates. Further work is warranted to address the possibility and implications that prostaglandins might not be cleared at a proper rate in AD brains. (C) 2008 Elsevier B.V. All rights reserved.