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標題: Japanese encephalitis virus down-regulates thioredoxin and induces ROS-mediated ASK1-ERK/p38 MAPK activation in human promonocyte cells
作者: Yang, T.C.
Lai, C.C.
Shiu, S.L.
Chuang, P.H.
Tzou, B.C.
Lin, Y.Y.
Tsai, F.J.
Lin, C.W.
關鍵字: Japanese encephalitis virus;Apoptosis;Oxidative stress;ER stress;Thioredoxin;ASK1;ERK1/2;p38 MAPK;endoplasmic-reticulum stress;erk1/2 activation;oxidative stress;neuronal death;up-regulation;infection;apoptosis;pathway;protects;proliferation
Project: Microbes and Infection
期刊/報告no:: Microbes and Infection, Volume 12, Issue 8-9, Page(s) 643-651.
Japanese encephalitis virus (JEV), a mosquito-borne flavivirus, causes severe neurological disease with high mortality. Molecular mechanisms of JEV pathogenesis such as upstream apoptotic processes and pathways are not yet completely resolved or understood. In this study, JEV replication in human promonocyte cells induced time-dependent apoptosis and activated virus dose-dependent caspases 3, 8 and 9. Proteomic analysis demonstrated up- and down-regulated (more or less than 1.5-fold) proteins in JEV-infected promonocyte cells. Biological process categorization showed processes of antioxidation, free radical removal, and sulfur redox metabolism entailed many identified up- and down-regulated proteins. Down-regulation of thioredoxin, confirmed by using Western blotting, was involved in the apoptosis process of the oxidative stress response pathway. JEV infection caused increased intracellular ROS production and activation of ASK1-ERK/p38 MAPK signaling. ERK/p38 MAPK inhibitor PD98059 treatment definitely suppressed this apoptosis. Down-regulation of thioredoxin, increased intracellular ROS, and activation of ASK1-ERK/p38 MAPK signaling all were associated with JEV-induced apoptosis. These results are suggestive of an oxidative stress-pathway as a key element of JE pathogenesis. Crown Copyright (c) 2010 Published by Elsevier Masson SAS. All rights reserved.
ISSN: 1286-4579
DOI: 10.1016/j.micinf.2010.04.007
Appears in Collections:分子生物學研究所

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