In vitro optimization of retinoic acid–induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox

Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in...

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Veröffentlicht in:Molecular and cellular biochemistry 2011-12, Vol.358 (1-2), p.325-334
Hauptverfasser: Frota Junior, Mario Luiz Conte da, Pires, André Simões, Zeidán-Chuliá, Fares, Bristot, Ivi Juliana, Lopes, Fernanda M., de Bittencourt Pasquali, Matheus Augusto, Zanotto-Filho, Alfeu, Behr, Guilherme Antônio, Klamt, Fabio, Gelain, Daniel Pens, Moreira, José Cláudio Fonseca
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container_issue 1-2
container_start_page 325
container_title Molecular and cellular biochemistry
container_volume 358
creator Frota Junior, Mario Luiz Conte da
Pires, André Simões
Zeidán-Chuliá, Fares
Bristot, Ivi Juliana
Lopes, Fernanda M.
de Bittencourt Pasquali, Matheus Augusto
Zanotto-Filho, Alfeu
Behr, Guilherme Antônio
Klamt, Fabio
Gelain, Daniel Pens
Moreira, José Cláudio Fonseca
description Though, it is quite well-known how retinoic acid (RA) is able to induce neuritogenesis in different in vitro models, the putative role exerted by reactive oxygen species (ROS) during this process still need to be further studied. For such purpose, we used a neuronal-like cell line (SH-SY5Y cells) in order to investigate whether the antioxidant Trolox (a hydrophilic analog of alpha-tocopherol) could have any effect on the number of RA-induced neurites, and how significant changes in cellular redox homeostasis may affect the cellular endogenous expression of tyrosine hydroxylase (TH). Our results show a significant enhancement of RA (10 μM)-induced neuritogenesis and TH endogenous expression, when cells were co-treated with Trolox (100 μM) for 7 days. Moreover, this effect was associated with an improvement in cellular viability. The mechanism seems to mainly involve PI3 K/Akt rather than MEK signaling pathway. Therefore, our data demonstrate that concomitant decreases in basal reactive oxygen species (ROS) production could exert a positive effect on the neuritogenic process of RA-treated SH-SY5Y cells.
doi_str_mv 10.1007/s11010-011-0983-2
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subjects Analysis
Antioxidants
Antioxidants - pharmacology
Biochemistry
Biomedical and Life Sciences
Cardiology
Cell Line, Tumor
Cell Survival - drug effects
Cellular biology
Chromans - pharmacology
Homeostasis
Humans
Indexing in process
Life Sciences
Lipid Peroxidation - drug effects
Medical Biochemistry
Microscopy, Phase-Contrast
Neurites - drug effects
Neurites - metabolism
Neuroblastoma - enzymology
Neuroblastoma - pathology
Neurogenesis - drug effects
Oncology
Oxidative Stress - drug effects
Parkinson's disease
Phosphatidylinositol 3-Kinases - antagonists & inhibitors
Phosphatidylinositol 3-Kinases - metabolism
Protein Kinase Inhibitors - pharmacology
Proto-Oncogene Proteins c-akt - antagonists & inhibitors
Proto-Oncogene Proteins c-akt - metabolism
Reactive Oxygen Species - metabolism
Tocopherols
Toy industry
Tretinoin
Tretinoin - pharmacology
Tyrosine 3-Monooxygenase - metabolism
title In vitro optimization of retinoic acid–induced neuritogenesis and TH endogenous expression in human SH-SY5Y neuroblastoma cells by the antioxidant Trolox
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