Retinol induces the ERK1/2-dependent phosphorylation of CREB through a pathway involving the generation of reactive oxygen species in cultured Sertoli cells

Cellular Signalling
Daniel P GelainJosé Cláudio F Moreira

Abstract

The ability to regulate cell cycle progression and apoptosis through the activation of nuclear receptors and gene transcription has been generally accepted as a potential chemopreventive and therapeutic property of retinoids. However, recent studies suggest that retinol and related compounds can exert rapid and non-genomic effects, which may increase the production of reactive oxygen species (ROS) and lead to cell cycle disruption and malignant transformation. In this work, we report that, in Sertoli cells, retinol (7 microM) induces the Src-dependent activation of ERK1/2 MAPK and the ERK1/2-mediated phosphorylation of the transcription factor CREB. We found that these retinol-induced effects were completely blocked by the antioxidant Trolox 100 microM (a hydrophilic analogue of alpha-tocopherol), the hydroxyl radical scavenger mannitol (1 mM) and the addition of native superoxide dismutase (200 U/ml), and also that retinol increased the production of ROS and several other parameters indicative of oxidative stress during the same incubation periods in which ERK1/2 and CREB were phosphorylated. The activation of the ERK1/2-CREB pathway appears to be involved in the onset of some of the malignant effects caused by retinol in Sert...Continue Reading

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Citations

Jun 6, 2008·Chemico-biological Interactions·Daniel Pens GelainJosé Cláudio Fonseca Moreira
Jan 1, 2010·Journal of Medicinal Food·Matheus Augusto de Bittencourt PasqualiJosé Cláudio Fonseca Moreira
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Jun 24, 2008·Free Radical Research·Alfeu Zanotto-FilhoJosé Cláudio F Moreira
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Nov 14, 2015·Applied Physiology, Nutrition, and Metabolism = Physiologie Appliquée, Nutrition Et Métabolisme·Juciano GasparottoDaniel Pens Gelain
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