Cortisol rapidly suppresses intracellular calcium and voltage-gated calcium channel activity in prolactin cells of the tilapia (<i>Oreochromis mossambicus</i>)

Hyde, Gregory N.; Seale, André P.; Grau, E. Gordon; Borski, Russell J.

doi:10.1152/ajpendo.00088.2003

Cited by 28 publications

(18 citation statements)

References 58 publications

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“…Corticosteroids may also exert rapid and/or non-genomic effects on ion transport (see Sakamoto et al (2001) and McCormick & Bradshaw (2006)) as has been demonstrated for aldosterone on ion regulation in tetrapods (see Harvey et al (2002)). In fish, rapid effects of glucocorticoids have been reported with regard to inhibition of pituitary prolactin release in tilapia (Borski et al 2001, Hyde et al 2004, lipogenic enzyme activity in tilapia liver cells (Sunny et al 2002) and on Na C ,K C -ATPase activity in the eel and tilapia gill (Marsigliante et al 2000, Sunny & Oommen 2001. We demonstrate in this study that both cortisol and DOC may rapidly affect (within 30 min) the MAPK signalling cascade via an increase in the phosphorylation state of ERK1 and ERK2.…”

Section: Rapid Effects Of Corticosteroidssupporting

confidence: 55%

Differential effects of cortisol and 11-deoxycorticosterone on ion transport protein mRNA levels in gills of two euryhaline teleosts, Mozambique tilapia (Oreochromis mossambicus) and striped bass (Morone saxatilis)

Kiilerich¹,

Tipsmark²,

Borski³

et al. 2011

Journal of Endocrinology

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The role of cortisol as the only corticosteroid in fish osmoregulation has recently been challenged with the discovery of a mineralocorticoid-like hormone, 11-deoxycorticosterone (DOC), and necessitates new studies of the endocrinology of osmoregulation in fish. Using an in vitro gill explant incubation approach, DOC-mediated regulation of selected osmoregulatory target genes in the gill was investigated and compared with that of cortisol in two euryhaline teleosts, Mozambique tilapia (Oreochromis mossambicus) and striped bass (Morone saxatilis). The effects were tested in gills from both fresh water (FW)-and seawater (SW)-acclimated fish. Both cortisol and DOC caused an up-regulation of the Na C ,K C -ATPase a1 subunit in SW-acclimated tilapia but had no effect in FW-acclimated fish. Cortisol conferred an increase in NaK cotransporter (NKCC) isoform 1a transcript levels in FW-and SW-acclimated tilapia, whereas DOC had a stimulatory effect only in SW-acclimated fish. Cortisol had no effect on NKCC isoform 1b mRNA levels at both salinities, while DOC stimulated this isoform in SW-acclimated fish. In striped bass, cortisol conferred an up-regulation of Na C ,K C -ATPase a1 and NKCC transcript levels in FW-and SW-acclimated fish, whereas DOC resulted in down-regulation of these transcripts in FW-acclimated fish. It was also found that both corticosteroids may rapidly (30 min) alter the mitogen-activated protein kinase signalling pathway in gill, inducing phosphorylation of extracellular signalregulated kinase 1 (ERK1) and ERK2 in a salinity-dependent manner. The study shows a disparate organisation of corticosteroid signalling mechanisms involved in ion regulation in the two species and adds new evidence to a role of DOC as a mineralocorticoid hormone in teleosts.

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Section: Rapid Effects Of Corticosteroidssupporting

confidence: 55%

Differential effects of cortisol and 11-deoxycorticosterone on ion transport protein mRNA levels in gills of two euryhaline teleosts, Mozambique tilapia (Oreochromis mossambicus) and striped bass (Morone saxatilis)

Kiilerich¹,

Tipsmark²,

Borski³

et al. 2011

Journal of Endocrinology

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“…A rapid action of glucocorticoids on Leydig cell function was also demonstrated. A rapid (30-min) decline of testosterone production was seen in mouse Leydig cells when these cells were exposed to 1.44 µM corticosterone (CORT), indicating that a non-genomic mechanism of glucocorticoids in Leydig cells [28], since the genomic mechanism of glucocorticoids requires hours to register at the protein level [29]. CORT can inhibit cAMP formation in mouse Leydig cells within 15 min [28].…”

Section: Rapid Glucocorticoid Actions Via Membrane Receptorsmentioning

confidence: 99%

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Lian

Lin

et al. 2008

Steroids

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Stress-mediated elevations in circulating glucocorticoid levels lead to corresponding rapid declines in testosterone production by Leydig cells in the testis. In previous studies we have established that glucocorticoids act on Leydig cells directly, through the classic glucocorticoid receptor (GR), and that access to the GR is controlled prior to the GR by a metabolizing pathway mediated by the type 1 isoform of 11β-hydroxysteroid dehydrogenase (11βHSD1). This enzyme is bidirectional (with both oxidase and reductase activities) and in the rat testis is exclusively localized in Leydig cells where it is abundantly expressed and may catalyze the oxidative inactivation of glucocorticoids. The predominant reductase direction of 11βHSD1 activity in liver cells is determined by an enzyme, hexose-6-phosphate dehydrogenase (H6PDH), on the luminal side of the smooth endoplasmic reticulum (SER). Generation of the pyridine nucleotide cofactor NADPH by H6PDH stimulates the reductase direction of 11βHSD1 resulting in increased levels of active glucocorticoids in liver cells. Unlike liver cells, steroidogenic enzymes including 17β-hydroxysteroid dehydrogenase 3 (17βHSD3) forms the coupling with 11βHSD1. Thus the physiological concentrations of androstenedione serve as a substrate for 17βHSD3 utilizing NADPH to generate NADP+, which drives 11βHSD1 in Leydig cells primarily as an oxidase; thus eliminating the adverse effects of glucocorticoids on testosterone production. At the same time 11βHSD1 generates NADPH which promotes testosterone biosynthesis by stimulating 17βHSD3 in a cooperative cycle. This enzymatic coupling constitutes a rapid mechanism for modulating glucocorticoid control of testosterone biosynthesis. Under stress conditions, glucocorticoids also have rapid actions to suppress cAMP formation thus to lower testosterone production.

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“…While the most rapid genomic effect reported for glucocorticoids takes little more than 7 minutes, such as in the case of the glucocorticoid-induced transcription of the mouse mammary tumor virus long terminal repeat in L tk2 aprt2 cells (Groner et al, 1983), genomic glucocorticoid actions usually require more than an hour before they are detectable (Joels and De Kloet, 1992). Non-genomic effects of glucocorticoids, on the other hand, occur more rapidly, often taking only seconds to minutes to be detected (Ffrench-Mullen, 1995;Hyde et al, 2004;Malcher-Lopes et al, 2006). The non-genomic actions of glucocorticoids may involve multiple mechanisms mediated by intracellular and/or membrane-associated receptors.…”

Section: Introductionmentioning

confidence: 99%

Glucocorticoids shift arachidonic acid metabolism toward endocannabinoid synthesis: A non-genomic anti-inflammatory switch

Malcher‐Lopes

Franco

Tasker

2008

European Journal of Pharmacology

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Glucocorticoids are capable of exerting both genomic and non-genomic actions in target cells of multiple tissues, including the brain, which trigger an array of electrophysiological, metabolic, secretory and inflammatory regulatory responses. Here, we have attempted to show how glucocorticoids may generate a rapid anti-inflammatory response by promoting arachidonic acidderived endocannabinoid biosynthesis. According to our hypothesized model, non-genomic action of glucocorticoids results in the global shift of membrane lipid metabolism, subverting metabolic pathways toward the synthesis of the anti-inflammatory endocannabinoids, anandamide (AEA) and 2-arachidonoyl-glycerol (2-AG), and away from arachidonic acid production. Post-transcriptional inhibition of cyclooxygenase-2 (COX 2 ) synthesis by glucocorticoids assists this mechanism by suppressing the synthesis of pro-inflammatory prostaglandins as well as endocannabinoid-derived prostanoids. In the central nervous system (CNS) this may represent a major neuroprotective system, which may cross-talk with leptin signaling in the hypothalamus allowing for the coordination between energy homeostasis and the inflammatory response.

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Cortisol rapidly suppresses intracellular calcium and voltage-gated calcium channel activity in prolactin cells of the tilapia (Oreochromis mossambicus)

Abstract: . Cortisol rapidly suppresses intracellular calcium and voltage-gated calcium channel activity in prolactin cells of the tilapia (Oreochromis mossambicus). Am J Physiol Endocrinol Metab

Cited by 28 publications

References 58 publications

Differential effects of cortisol and 11-deoxycorticosterone on ion transport protein mRNA levels in gills of two euryhaline teleosts, Mozambique tilapia (Oreochromis mossambicus) and striped bass (Morone saxatilis)

Differential effects of cortisol and 11-deoxycorticosterone on ion transport protein mRNA levels in gills of two euryhaline teleosts, Mozambique tilapia (Oreochromis mossambicus) and striped bass (Morone saxatilis)

Rapid mechanisms of glucocorticoid signaling in the Leydig cell☆

Glucocorticoids shift arachidonic acid metabolism toward endocannabinoid synthesis: A non-genomic anti-inflammatory switch

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