Induction of rat L-phosphoserine phosphatase by amyloid-β (1-42) is inhibited by interleukin-11
Induction of rat L-phosphoserine phosphatase by amyloid-β (1-42) is inhibited by interleukin-11
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DOI：
10.1016/s0304-3940(00)01197-6
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发表时间：
2000-07-07
影响因子：
2.5
通讯作者：
Sawada, T
中科院分区：
文献类型：
--
作者：
Heese, K;Nagai, Y;Sawada, T
阿尔茨海默病（AD）的特点是大脑中存在β -淀粉样蛋白（A β）沉积，A β(1-42)肽产生增加被认为是AD发病机制的早期事件之一，导致进行性神经退行性过程和痴呆。利用cDNA减法和逆转录聚合酶链反应，我们检测了A β(1-42)肽诱导的大鼠神经母细胞瘤B104细胞的基因表达。此外，我们假设白细胞介素-11 （IL-11）支持神经元存活。我们发现A β(1-42)激活了神经元细胞中被IL-11抑制的l -磷酸丝氨酸磷酸酶。此外，IL-11以剂量依赖的方式抑制A β(1-42)诱导的神经毒性。我们的研究表明，l -磷酸丝氨酸磷酸酶可能通过增强谷氨酸诱导的神经毒性在AD的神经元功能改变中发挥作用，IL-11受体系统可能在人脑中发挥神经保护细胞因子的作用。(C) 2000爱思唯尔科学爱尔兰有限公司版权所有。
Alzheimer's disease (AD) is characterized by the presence of beta-amyloid (A beta) protein deposits in the brain and increased A beta (1-42) peptide production is thought to be one of the early events in the pathogenesis of AD that leads to progressive neurodegenerative processes and dementia. Using cDNA subtraction and reverse transcription-polymerase chain reaction, we examined the A beta (1-42) peptide-induced gene expression in rat neuroblastoma B104 cells. In addition we hypothesized that interleukin-11 (IL-11) supports neuronal survival. We found that A beta (1-42) activates L-phosphoserine phosphatase in neuronal cells which is inhibited by IL-11. Moreover, IL-11 inhibits A beta (1-42)-induced neurotoxicity in a dose-dependent manner. Our study suggests that L-phosphoserine phosphatase may play a role in altered neuronal function in AD via enhancing glutamate-induced neurotoxicity by D-serine and the IL-11 receptor system may act as a neuroprotective cytokine in human brain. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.