Amyloid-β peptides induce several chemokine mRNA expressions in the primary microglia and Ra2 cell line via the PI3K/Akt and/or ERK pathway
Amyloid-β peptides induce several chemokine mRNA expressions in the primary microglia and Ra2 cell line via the PI3K/Akt and/or ERK pathway
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DOI：
10.1016/j.neures.2006.07.009
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发表时间：
2006-11-01
影响因子：
2.9
通讯作者：
Isobe, Ken-ichi
中科院分区：
文献类型：
--
作者：
Ito, Sachiko;Sawada, Makoto;Isobe, Ken-ichi
Alzheimer's disease (AD) is characterized by the presence of senile plaques composed primarily of amyloid-beta peptide (A beta) in the brain. Microglia have been reported to surround these A beta plaques, which have opposite roles, provoking a microglia-mediated inflammatory response that contributes to neuronal cell loss or the removal of A beta and damaged neurons. To perform these tasks microglia migrate to the sites of A beta secretion. We herein analyzed the process of chemokine expression induced by A beta stimulation in primary murine microglia and Ra2 microglial cell line. We found that A beta 1-42 induced the expressions of CCL7, CCL2, CCL3, CCL4 and CXCL2 in the microglia. The signal transduction pathway for the expression of CCL2 and CCL7 mRNA induced by A beta 1-42 was found to depend on phosphatidylinositol 3-kinase (PI3K)/Akt and extracellular signal-regulated kinase (ERK), whereas the pathway for CCL4 depended only on PI3K/Akt. These inflammatory chemokine expressions by A beta stimulation emphasize the contribution of neuroinflammatory mechanisms to the pathogenesis of AD. (c) 2006 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
