Role of glucocorticoid receptor in acclimation of killifish (Fundulus heteroclitus) to seawater and effects of arsenic.

Article Details

Citation

Shaw JR, Gabor K, Hand E, Lankowski A, Durant L, Thibodeau R, Stanton CR, Barnaby R, Coutermarsh B, Karlson KH, Sato JD, Hamilton JW, Stanton BA

Role of glucocorticoid receptor in acclimation of killifish (Fundulus heteroclitus) to seawater and effects of arsenic.

Am J Physiol Regul Integr Comp Physiol. 2007 Feb;292(2):R1052-60. Epub 2006 Oct 12.

PubMed ID
17038445 [ View in PubMed
]
Abstract

Killifish are euryhaline teleosts that adapt to rapid changes in the salinity of the seawater. It is generally accepted that acclimation to seawater is mediated by cortisol activation of the glucocorticoid receptor (GR), which stimulates CFTR mRNA expression and CFTR-mediated Cl- secretion by the gill. Because there is no direct evidence in killifish that the GR stimulates CFTR gene expression, quantitative PCR studies were conducted to test the hypothesis that cortisol activation of GR upregulates CFTR mRNA expression and that this response is required for acclimation to seawater. Inhibition of the GR by RU-486 prevented killifish from acclimating to increased salinity and blocked the increase in CFTR mRNA. In contrast, inhibition of the mineralocorticoid receptor by spironolactone had no effect on acclimation to seawater. Thus acclimation to increased salinity in killifish requires signaling via the GR and includes an increase in CFTR gene expression. Because arsenic, a toxic metalloid that naturally occurs in the aquatic environment, has been shown to disrupt GR transcriptional regulation in avian and mammalian systems, studies were also conducted to determine whether arsenic disrupts cortisol-mediated activation of CFTR gene expression in this in vivo fish model and thereby blocks the ability of killifish to acclimate to increased salinity. Arsenic prevented acclimation to seawater and decreased CFTR protein abundance. However, arsenic did not disrupt the GR-induced increase in CFTR mRNA. Thus arsenic blocks acclimation to seawater in killifish by a mechanism that does not disrupt GR-mediated induction of CFTR gene expression.

DrugBank Data that Cites this Article

Drug Targets
DrugTargetKindOrganismPharmacological ActionActions
AmcinonideGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
Cortisone acetateGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
DesonideGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
DesoximetasoneGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
FluorometholoneGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
HydrocortisoneGlucocorticoid receptorProteinHumans
Yes
Agonist
Details
Hydrocortisone aceponateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone acetateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone butyrateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone cypionateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone phosphateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone probutateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
Hydrocortisone valerateGlucocorticoid receptorProteinHumans
Yes
Not AvailableDetails
ParamethasoneGlucocorticoid receptorProteinHumans
Yes
Agonist
Details