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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Reactive Oxygen Species (ROS) Are Not a Key Determinant for Zika Virus-Induced Apoptosis in SH-SY5Y Neuroblastoma Cells

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Author(s):
de Mendonca-Vieira, Leila Rodrigues [1] ; Anibal-Silva, Conceicao Elidianne [2] ; Menezes-Neto, Armando [1] ; Neves Azevedo, Elisa de Almeida [1] ; Zanluqui, Nagela Ghabdan [3] ; Schatzmann Peron, Jean Pierre [3] ; de Oliveira Franca, Rafael Freitas [1]
Total Authors: 7
Affiliation:
[1] Oswaldo Cruz Fdn Fiocruz, Aggeu Magalhaes Inst, BR-50740465 Recife, PE - Brazil
[2] Univ Sao Paulo, Ribeirao Preto Med Sch, BR-14049900 Ribeirao Preto - Brazil
[3] Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, BR-05508000 Sao Paulo - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Viruses-Basel; v. 13, n. 11 NOV 2021.
Web of Science Citations: 0
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. (AU)

FAPESP's process: 16/07371-2 - Characterization of the role of T CD8+ lymphocytes in Zika virus infection
Grantee:Nagela Ghabdan Zanluqui
Support Opportunities: Scholarships in Brazil - Doctorate
FAPESP's process: 17/22504-1 - TAM receptors and their ligands Gas6 and Pros1 on the ZIKV Congenital Syndrome in Experimental Models
Grantee:Jean Pierre Schatzmann Peron
Support Opportunities: Regular Research Grants
FAPESP's process: 17/26170-0 - Neuroimmunology in experimental models of Autoimmune Encephalomyelitis and Congenital Zika Syndrome: physiopathogenesis, susceptibility, cellular therapy, vaccination
Grantee:Carolina Demarchi Munhoz
Support Opportunities: Research Projects - Thematic Grants