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@ARTICLE{AlpucheLazcano:284083,
author = {Alpuche-Lazcano, Sergio P. and Saliba, James and Costa,
Vivian V. and Campolina-Silva, Gabriel H. and Marim,
Fernanda M. and Secchim Ribeiro, Lucas and Blank, Volker and
Mouland, Andrew J. and Teixeira, Mauro M. and Gatignol,
Anne},
title = {{P}rofound downregulation of neural transcription factor
{N}pas4 and {N}r4a family in fetal mice neurons infected
with {Z}ika virus},
journal = {PLoS neglected tropical diseases},
volume = {15},
number = {5},
issn = {1935-2727},
address = {Lawrence, Kan.},
publisher = {PLoS},
reportid = {DZNE-2026-00091},
pages = {e0009425},
year = {2021},
abstract = {Zika virus (ZIKV) infection of neurons leads to
neurological complications and congenital malformations of
the brain of neonates. To date, ZIKV mechanism of infection
and pathogenesis is not entirely understood and different
studies on gene regulation of ZIKV-infected cells have
identified a dysregulation of inflammatory and stem cell
maintenance pathways. MicroRNAs (miRNAs) are
post-transcriptional regulators of cellular genes and they
contribute to cell development in normal function and
disease. Previous reports with integrative analyses of
messenger RNAs (mRNAs) and miRNAs during ZIKV infection have
not identified neurological pathway defects. We hypothesized
that dysregulation of pathways involved in neurological
functions will be identified by RNA profiling of
ZIKV-infected fetal neurons. We therefore used microarrays
to analyze gene expression levels following ZIKV infection
of fetal murine neurons. We observed that the expression
levels of transcription factors such as neural PAS domain
protein 4 (Npas4) and of three members of the orphan nuclear
receptor 4 (Nr4a) were severely decreased after viral
infection. We confirmed that their downregulation was at
both the mRNA level and at the protein level. The
dysregulation of these transcription factors has been
previously linked to aberrant neural functions and
development. We next examined the miRNA expression profile
in infected primary murine neurons by microarray and found
that various miRNAs were dysregulated upon ZIKV infection.
An integrative analysis of the differentially expressed
miRNAs and mRNAs indicated that miR-7013-5p targets Nr4a3
gene. Using miRmimics, we corroborated that miR-7013-5p
downregulates Nr4a3 mRNA and protein levels. Our data
identify a profound dysregulation of neural transcription
factors with an overexpression of miR-7013-5p that results
in decreased Nr4a3 expression, likely a main contributor to
ZIKV-induced neuronal dysfunction.},
keywords = {Animals / Basic Helix-Loop-Helix Transcription Factors:
genetics / Basic Helix-Loop-Helix Transcription Factors:
metabolism / Cell Line, Tumor / Cells, Cultured /
Down-Regulation / Embryo, Mammalian: virology / Gene
Expression Profiling / Mice / MicroRNAs: genetics / Neurons:
metabolism / Orphan Nuclear Receptors: genetics / Orphan
Nuclear Receptors: metabolism / RNA, Messenger: genetics /
Transcription Factors: genetics / Transcription Factors:
metabolism / Zika Virus: pathogenicity / Zika Virus
Infection: pathology / Basic Helix-Loop-Helix Transcription
Factors (NLM Chemicals) / MicroRNAs (NLM Chemicals) / Npas4
protein, mouse (NLM Chemicals) / Orphan Nuclear Receptors
(NLM Chemicals) / RNA, Messenger (NLM Chemicals) /
Transcription Factors (NLM Chemicals)},
ddc = {610},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
doi = {10.1371/journal.pntd.0009425},
url = {https://pub.dzne.de/record/284083},
}