Please use this identifier to cite or link to this item: http://hdl.handle.net/1893/1705
Appears in Collections:Aquaculture Journal Articles
Peer Review Status: Refereed
Title: Cortisol stimulates the zinc signaling pathway and expression of metallothioneins and ZnT1 in rainbow trout gill epithelial cells
Author(s): Bury, Nicholas R
Chung, Mi Ja
Sturm, Armin
Walker, Paul A
Hogstrand, Christer
Contact Email: as49@stir.ac.uk
Keywords: fish
metals
glucocorticoid receptor
Rainbow trout Anatomy
Glucocorticoids Receptors
Issue Date: Feb-2008
Date Deposited: 15-Oct-2009
Citation: Bury NR, Chung MJ, Sturm A, Walker PA & Hogstrand C (2008) Cortisol stimulates the zinc signaling pathway and expression of metallothioneins and ZnT1 in rainbow trout gill epithelial cells. American Journal of Physiology - Regulatory, Integrative and Comparative Physiology, 294 (2), pp. R623-R629. http://ajpregu.physiology.org/; https://doi.org/10.1152/ajpregu.00646.2007
Abstract: Intracellular zinc signaling is important in the control of a number of cellular processes. Hormonal factors that regulate cellular zinc influx and initiate zinc signals are poorly understood. The present study investigates the possibility for cross talk between the glucocorticoid and zinc signaling pathways in cultured rainbow trout gill epithelial cells. The rainbow trout metallothionein A (MTA) gene possesses a putative glucocorticoid response element and multiple metal response elements 1042 base pairs upstream of the start codon, whereas metallothionein B (MTB) and zinc transporter-1 (ZnT1) have multiple metal response elements but no glucocorticoid response elements in this region. Cortisol increased MTA, MTB, and ZnT1 gene expression, and this stimulation was enhanced if cells were treated with cortisol together with zinc. Cells treated with zinc showed increased zinc accumulation, transepithelial zinc influx (apical to basolateral), and intracellular labile zinc concentrations. These responses were also significantly enhanced in cells pretreated with cortisol and zinc. The cortisol-mediated effects were blocked by the glucocorticoid receptor (GR) antagonist RU-486, indicating mediation via a GR. In reporter gene assays, zinc stimulated MTA promoter activity, whereas cortisol did not. Furthermore, cortisol significantly reduced zinc-stimulated MTA promoter activity in cells expressing exogenous rainbow trout GR. These results demonstrate that cortisol enhances cellular zinc uptake, which in turn stimulates expression of MTA, MTB, and ZnT1 genes.
URL: http://ajpregu.physiology.org/
DOI Link: 10.1152/ajpregu.00646.2007
Rights: Copyright by American Physiological Society; The publisher does not allow this work to be made publicly available in this Repository. Please use the Request a Copy feature at the foot of the Repository record to request a copy directly from the author; you can only request a copy if you wish to use this work for your own research or private study.
Licence URL(s): http://www.rioxx.net/licenses/under-embargo-all-rights-reserved

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