Amar NagilaJanjuree NetsawangChatchawan SrisawatSansanee NoisakranAtthapan MorchangUmpa YasamutChunya PuttikhuntWatchara KasinrerkPrida MalasitPa thai YenchitsomanusThawornchai LimjindapornMahidol UniversityRangsit UniversityThailand National Center for Genetic Engineering and BiotechnologyChiang Mai University2018-05-032018-05-032011-07-08Biochemical and Biophysical Research Communications. Vol.410, No.3 (2011), 428-433109021040006291X2-s2.0-79960050971https://repository.li.mahidol.ac.th/handle/20.500.14594/11515Hepatic dysfunction is a well recognized feature of dengue virus (DENV) infection. However, molecular mechanisms of hepatic injury are still poorly understood. A complex interaction between DENV and the host immune response contributes to DENV-mediated tissue injury. DENV capsid protein (DENV C) physically interacts with the human death domain-associated protein Daxx. A double substitution mutation in DENV C (R85A/K86A) abrogates Daxx interaction, nuclear localization and apoptosis. Therefore we compared the expression of cell death genes between HepG2 cells expressing DENV C and DENV C (R85A/K86A) using a real-time PCR array. Expression of CD137, which is a membe r of the tumor necrosis factor receptor family, increased significantly in HepG2 cells expressing DENV C compared to HepG2 cells expressing DENV C (R85A/K86A). In addition, CD137-mediated apoptotic activity in HepG2 cells expressing DENV C was significantly increased by anti-CD137 antibody compared to that of HepG2 cells expressing DENV C (R85A/K86A). In DENV-infected HepG2 cells, CD137 mRNA and CD137 positive cells significantly increased and CD137-mediated apoptotic activity was increased by anti-CD137 antibody. This work is the first to demonstrate the contribution of CD137 signaling to DENV-mediated apoptosis. © 2011 Elsevier Inc.Mahidol UniversityBiochemistry, Genetics and Molecular BiologyArticleSCOPUS10.1016/j.bbrc.2011.05.151