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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/35574
Title: NF-κB is required for dengue virus NS5-induced RANTES expression
Authors: Sasiprapa Khunchai
Mutita Junking
Aroonroong Suttitheptumrong
Suwattanee Kooptiwut
Guy Haegeman
Thawornchai Limjindaporn
Pa Thai Yenchitsomanus
Mahidol University
Faculty of Pharmaceutical Sciences
Keywords: Biochemistry, Genetics and Molecular Biology;Immunology and Microbiology;Medicine
Issue Date: 1-Jan-2015
Citation: Virus Research. Vol.197, (2015), 92-100
Abstract: © 2014 Elsevier B.V. Dengue virus (DENV) infection associates with renal disorders. Patients with dengue hemorrhagic fever and acute kidney injury have a high mortality rate. Increased levels of cytokines may contribute to the pathogenesis of DENV-induced kidney injury. Currently, molecular mechanisms how DENV induces kidney cell injury has not been thoroughly investigated. Excessive cytokine production may be involved in this process. Using human cytokine RT2Profiler PCR array, 14 genes including IP-10, RANTES, IL-8, CXCL-9 and MIP-1β were up-regulated more than 2folds in DENV-infected HEK 293 cells compared to that of mock-infected HEK 293 cells. In the present study, RANTES was suppressed by the NF-κB inhibitor, compound A (CpdA), in DENV-infected HEK 293 cells implying the role of NF-κB in RANTES expression. Chromatin immunoprecipitation (ChIP) assay showed that NF-κB binds more efficiently to its binding sites on the RANTES promoter in NS5-transfected HEK 293 cells than in HEK 293 cells expressing the vector lacking NS5 gene. To further examine whether the NS5-activated RANTES promoter is mediated through NF-κB, the two NF-κB binding sites on the RANTES promoter were mutated and this promoter was coupled to the luciferase cDNA. The result showed that when both binding sites of NF-κB in the RANTES promoter were mutated, the ability of NS5 to induce the luciferase activity was significantly decreased. Therefore, DENV NS5 activates RANTES production by increasing NF-κB binding to its binding sites on the RANTES promoter.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=84922769366&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/35574
ISSN: 18727492
01681702
Appears in Collections:Scopus 2011-2015

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