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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/33234
Title: Role of ERK1/2 signaling in dengue virus-induced liver injury
Authors: Gopinathan Pillai Sreekanth
Aporn Chuncharunee
Aunchalee Sirimontaporn
Jutatip Panaampon
Chatchawan Srisawat
Atthapan Morchang
Shilu Malakar
Peti Thuwajit
Suwattanee Kooptiwut
Aroonroong Suttitheptumrong
Pucharee Songprakhon
Sansanee Noisakran
Pa thai Yenchitsomanus
Thawornchai Limjindaporn
Mahidol University
Thailand National Center for Genetic Engineering and Biotechnology
Keywords: Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology;Medicine
Issue Date: 8-Aug-2014
Citation: Virus Research. Vol.188, (2014), 15-26
Abstract: The liver is considered to be an important organ of dengue virus (DENV) replication and pathogenesis. However, molecular mechanisms of hepatic injury are still poorly understood. Modulation of Mitogen Activated Protein Kinases (MAPKs) was previously shown to affect DENV-induced apoptosis of hepatocytes in vitro. However, the in vivo role of ERK1/2, a member of the MAPK family, and the question whether its activation can facilitate cell survival or cell death, has not been thoroughly investigated. Therefore, the role of ERK1/2 in a mouse model of DENV infection was examined. Our results show that DENV induces phosphorylation of ERK1/2 and increases apoptosis. Inhibition of phosphorylated ERK1/2 by the selective ERK1/2 inhibitor, FR180204, limits hepatocyte apoptosis and reduces DENV-induced liver injury. Clinical parameters, including leucopenia, thrombocytopenia, transaminases and histology, show improvements after FR180204 treatment. The expression of cell death genes was further identified using real-time PCR array and Western blot analysis. Caspase-3 was significantly decreased in FR180204 treated DENV-infected mice compared to the levels of untreated DENV-infected mice suggesting the role of ERK1/2 signaling in immune-mediated liver injury during DENV infection. © 2014 Elsevier B.V.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84903708637&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/33234
ISSN: 18727492
01681702
Appears in Collections:Scopus 2011-2015

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