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Zika Virus Induces Tumor Necrosis Factor-Related Apoptosis Inducing Ligand (TRAIL)-Mediated Apoptosis in Human Neural Progenitor Cells.
Lee, Jae Kyung; Kim, Ji-Ae; Oh, Soo-Jin; Lee, Eun-Woo; Shin, Ok Sarah.
Afiliación
  • Lee JK; BK21 Graduate Program, Department of Biomedical Sciences, Korea University College of Medicine, Seoul 08308, Korea.
  • Kim JA; BK21 Graduate Program, Department of Biomedical Sciences, Korea University College of Medicine, Seoul 08308, Korea.
  • Oh SJ; BK21 Graduate Program, Department of Biomedical Sciences, Korea University College of Medicine, Seoul 08308, Korea.
  • Lee EW; Metabolic Regulation Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Korea.
  • Shin OS; BK21 Graduate Program, Department of Biomedical Sciences, Korea University College of Medicine, Seoul 08308, Korea.
Cells ; 9(11)2020 11 16.
Article en En | MEDLINE | ID: mdl-33207682
Zika virus (ZIKV) remains as a public health threat due to the congenital birth defects the virus causes following infection of pregnant women. Congenital microcephaly is among the neurodevelopmental disorders the virus can cause in newborns, and this defect has been associated with ZIKV-mediated cytopathic effects in human neural progenitor cells (hNPCs). In this study, we investigated the cellular changes that occur in hNPCs in response to ZIKV (African and Asian lineages)-induced cytopathic effects. Transmission electron microscopy showed the progress of cell death as well as the formation of numerous vacuoles in the cytoplasm of ZIKV-infected hNPCs. Infection with both African and Asian lineages of ZIKV induced apoptosis, as demonstrated by the increased activation of caspase 3/7, 8, and 9. Increased levels of proinflammatory cytokines and chemokines (IL-6, IL-8, IL-1ß) were also detected in ZIKV-infected hNPCs, while z-VAD-fmk-induced inhibition of cell death suppressed ZIKV-mediated cytokine production in a dose-dependent manner. ZIKV-infected hNPCs also displayed significantly elevated gene expression levels of the pro-apoptotic Bcl2-mediated family, in particular, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Furthermore, TRAIL signaling led to augmented ZIKV-mediated cell death and the knockdown of TRAIL-mediated signaling adaptor, FADD, resulted in enhanced ZIKV replication. In conclusion, our findings provide cellular insights into the cytopathic effects induced by ZIKV infection of hNPCs.
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Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Apoptosis / Factores de Necrosis Tumoral / Células-Madre Neurales / Virus Zika / Infección por el Virus Zika Límite: Humans / Newborn Idioma: En Revista: Cells Año: 2020 Tipo del documento: Article

Texto completo: 1 Bases de datos: MEDLINE Asunto principal: Apoptosis / Factores de Necrosis Tumoral / Células-Madre Neurales / Virus Zika / Infección por el Virus Zika Límite: Humans / Newborn Idioma: En Revista: Cells Año: 2020 Tipo del documento: Article