Evidence map›Paper›PMID 25465239›Full record

ArticleMolecular neurobiology2016

Gene Expression Profile of NF-κB, Nrf2, Glycolytic, and p53 Pathways During the SH-SY5Y Neuronal Differentiation Mediated by Retinoic Acid.

Matheus Augusto de Bittencourt Pasquali, Vitor Miranda de Ramos, Ricardo D Oliveira Albanus, Alice Kunzler, Luis Henrinque Trentin de Souza, Rodrigo Juliani Siqueira Dalmolin, Daniel Pens Gelain, Leila Ribeiro, Luigi Carro, José Cláudio Fonseca Moreira

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 24 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Matheus Augusto de Bittencourt PasqualiDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil. 00124262@ufrgs.br.
Vitor Miranda de RamosDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Ricardo D Oliveira AlbanusDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Alice KunzlerDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Luis Henrinque Trentin de SouzaDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Rodrigo Juliani Siqueira DalmolinDepartamento de Bioquímica, Instituto de Medicina Tropical, Universidade Federal do Rio Grande do Norte-UFRN, Avenida Senador Salgado Filho 3000, Cep 59078-900, Natal, Rio Grande do Norte, Brazil.
Daniel Pens GelainDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Leila RibeiroDepartamento de Informática Aplicada, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Bento Gonçalves 9500, Cep 91501-970, Porto Alegre, Rio Grande do Sul, Brazil.
Luigi CarroDepartamento de Informática Aplicada, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Bento Gonçalves 9500, Cep 91501-970, Porto Alegre, Rio Grande do Sul, Brazil.
José Cláudio Fonseca MoreiraDepartamento de Bioquímica, Centro de Estudos em Estresse Oxidativo, Universidade Federal do Rio Grande do Sul-UFRGS, Rua Ramiro Barcelos 2600, Cep 90035-003, Porto Alegre, Rio Grande do Sul, Brazil.
Universidade Federal do Rio Grande do Sul · BRUniversidade Federal do Rio Grande do Norte · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

SH-SY5Y cells, a neuroblastoma cell line that is a well-established model system to study the initial phases of neuronal differentiation, have been used in studies to elucidate the mechanisms of neuronal differentiation. In the present study, we investigated alterations of gene expression in SH-SY5Y cells during neuronal differentiation mediated by retinoic acid (RA) treatment. We evaluated important pathways involving nuclear factor kappa B (NF-κB), nuclear E2-related factor 2 (Nrf2), glycolytic, and p53 during neuronal differentiation. We also investigated the involvement of reactive oxygen species (ROS) in modulating the gene expression profile of those pathways by antioxidant co-treatment with Trolox®, a hydrophilic analogue of α-tocopherol. We found that RA treatment increases levels of gene expression of NF-κB, glycolytic, and antioxidant pathway genes during neuronal differentiation of SH-SY5Y cells. We also found that ROS production induced by RA treatment in SH-SY5Y cells is involved in gene expression profile alterations, chiefly in NF-κB, and glycolytic pathways. Antioxidant co-treatment with Trolox® reversed the effects mediated by RA NF-κB, and glycolytic pathways gene expression. Interestingly, co-treatment with Trolox® did not reverse the effects in antioxidant gene expression mediated by RA in SH-SY5Y. To confirm neuronal differentiation, we quantified endogenous levels of tyrosine hydroxylase, a recognized marker of neuronal differentiation. Our data suggest that during neuronal differentiation mediated by RA, changes in profile gene expression of important pathways occur. These alterations are in part mediated by ROS production. Therefore, our results reinforce the importance in understanding the mechanism by which RA induces neuronal differentiation in SH-SY5Y cells, principally due this model being commonly used as a neuronal cell model in studies of neuronal pathologies.

Indexed as

Gene Expression ProfilingCell DifferentiationCell Line, TumorGene Expression RegulationGene Regulatory NetworksGlycolysisHumansNeuronsNF-E2-Related Factor 2NF-kappa BSignal TransductionTretinoinTumor Suppressor Protein p53NFE2L2 protein, humanNF-E2-Related Factor 2NF-kappa BTretinoinTumor Suppressor Protein p53NeuroblastomaNeuronal differentiationOxidative stressRetinoic acidSH-SY5Y cells

Identifiers

PMID25465239
OpenAlexW2039259900

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.