Amyloid beta peptide and NMDA induce ROS from NADPH oxidase and AA release from cytosolic phospholipase A2 in cortical neurons

被引:230
作者
Shelat, Phullara B. [1 ]
Chalimoniuk, Malgorzata [1 ,2 ]
Wang, Jing-Hung [1 ]
Strosznajder, Joanna B. [2 ]
Lee, James C. [3 ]
Sun, Albert Y. [4 ]
Simonyi, Agnes [1 ]
Sun, Grace Y. [1 ]
机构
[1] Univ Missouri, Dept Biochem, Columbia, MO 65211 USA
[2] Polish Acad Sci, Med Res Ctr, Dept Cellular Signaling, Warsaw, Poland
[3] Univ Missouri, Dept Biol Engn, Columbia, MO 65211 USA
[4] Univ Missouri, Dept Med Pharmacol & Physiol, Columbia, MO 65211 USA
关键词
Alzheimer's disease; amyloid-beta peptide; arachidonic acid; cortical neurons; cytosolic phospholipase A(2)alpha; NADPH oxidase; NMDA; reactive oxygen species;
D O I
10.1111/j.1471-4159.2008.05347.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Increase in oxidative stress has been postulated to play an important role in he pathogenesis of a number of neurodegenerative diseases including Alzheimer's disease. There is evidence for involvement of amyloid-beta peptide (A beta) in mediating the oxidative damage to neurons. Despite yet unknown mechanism, A beta appears to exert action on the ionotropic glutamate receptors, especially the N-methyl-D-aspartic acid (NMDA) receptor subtypes. In this study, we showed that NMDA and oligomeric A beta(1-42) could induce reactive oxygen species (ROS) production from cortical neurons through activation of NADPH oxidase. ROS derived from NADPH oxidase led to activation of extracellular signal-regulated kinase 1/2, phosphorylation of cytosolic phospholipase A(2)alpha (cPLA(2)alpha), and arachidonic acid (AA) release. In addition, A beta(1-42)-induced AA release was inhibited by D(-)-2-amino-5-phosphonopentanoic acid and memantine, two different NMDA receptor antagonists, suggesting action of A beta through the NMDA receptor. Besides serving as a precursor for eicosanoids, AA is also regarded as a retrograde messenger and plays a role in modulating synaptic plasticity. Other phospholipase A(2) products such as lysophospholipids can perturb membrane phospholipids. These results suggest an oxidative-degradative mechanism for oligomeric A beta(1-42) to induce ROS production and stimulate AA release through the NMDA receptors. This novel mechanism may contribute to the oxidative stress hypothesis and synaptic failure that underline the pathogenesis of Alzheimer's disease.
引用
收藏
页码:45 / 55
页数:11
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