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https://www.arca.fiocruz.br/handle/icict/70247
REACTIVE OXYGEN SPECIES (ROS) ARE NOT A KEY DETERMINANT FOR ZIKA VIRUS-INDUCED APOPTOSIS IN SH-SY5Y NEUROBLASTOMA CELLS
Author
Affilliation
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil
Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Departamento de Imunologia. Instituto de Ciências Biomédicas. Universidade de São Paulo, São Paulo, Brasil.
Departamento de Imunologia. Instituto de Ciências Biomédicas. Universidade de São Paulo, São Paulo, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Departamento de Imunologia. Instituto de Ciências Biomédicas. Universidade de São Paulo, São Paulo, Brasil.
Departamento de Imunologia. Instituto de Ciências Biomédicas. Universidade de São Paulo, São Paulo, Brasil.
Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil.
Abstract
Introduction: ZIKV is a highly neurotropic virus that can cause the death of infected neuroprogenitor cells through mitochondrial damage and intrinsic apoptotic signaling. In this context, the role of reactive oxygen species (ROS) in neuronal cell death caused by ZIKV still remains elusive.
Objective: We aimed at evaluating the role of these cellular components in the death of human undifferentiated neuroblastoma cell line infected with ZIKV.
Results: ZIKV infection resulted in the extensive death of SH-SY5Y cells with the upregulation of several genes involved in survival and apoptotic responses as well as the colocalization of mitochondrial staining with ZIKV Envelope (E) protein. Notably, levels of intracellular reactive oxygen species (ROS) were not altered during ZIKV infection in undifferentiated SH-SY5Y cells, and consistent with these results, the treatment of infected cells with the widely studied ROS scavenger N-acetylcysteine (NAC) did not prevent cell death in these cells.
Conclusion: Altogether, our results suggest that excessive ROS production is not the main trigger of SH-SY5Y cells death in ZIKV infection.
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