Genomic and non-genomic effect of cortisol on phagocytosis in freshwater teleost Channa punctatus: An in vitro study

Roy, Brototi; Rai, Umesh

doi:10.1016/j.steroids.2008.12.013

Cited by 33 publications

(18 citation statements)

References 36 publications

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“…At the level of the pituitary in vitro, however, rapid inhibition of membrane potential (Hua and Chen, 1989) and ACTH release (Dayanithi and Antoni, 1989;John et al, 2002;Buckingham et al, 2003) occurs via a nongenomic Annexin 1-mediated GR mechanism (Taylor et al, 1993). Our data reveal a response that is more rapid than demonstrated for Annexin 1 and fits better with recent in vitro and in vivo evidence for rapid corticosteroid processes acting via a membrane-bound GR (Tait et al, 2008;Breuner and Orchinik, 2009;Roy and Rai, 2009), probably mediated through a phosphatidylinositol 3-kinase pathway (Limbourg et al, 2002;Matthews et al, 2008;Roy and Rai, 2009). This suggests a fast feedback inhibition that targets the fusion of ACTH-containing vesicles with the cell membrane and their subsequent release from corticotrophs and explains why the constitutive release of POMC was unaffected.…”

Section: Discussionsupporting

confidence: 84%

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

Russell¹,

Henley²,

Leendertz³

et al. 2010

J. Neurosci.

106

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A complex dynamic ultradian rhythm underlies the hypothalamic-pituitary-adrenal (HPA) circadian rhythm. We have investigated in normal human male subjects the importance, site of action, and receptor-mediated processes involved in rapid basal corticosteroid feedback and its interaction with corticotrophin releasing hormone (CRH) drive. Pro-opiomelanocortin (POMC), ACTH, and cortisol were measured every 10 min from healthy males during the awakening period or late afternoon using an automated blood sampling system. Mathematical modeling into discrete pulses of activity revealed that intravenous infusion of the synthetic mixed glucocorticoid/ mineralocorticoid agonist prednisolone produced rapid inhibition of ACTH and cortisol pulsatility within 30 min in the morning and afternoon. Any pulse that had commenced at the time of injection was unaffected, and subsequent pulsatility was inhibited. Prednisolone also inhibited ACTH and cortisol secretion in response to exogenous CRH stimulation, inferring rapid feedback inhibition at the anterior pituitary. Circulating POMC peptide concentrations were unaffected, suggesting that the rapid corticosteroid inhibitory effect specifically targeted ACTH secretion from pituitary corticotrophs. Prednisolone fast feedback was only reduced by glucocorticoid receptor antagonist pretreatment and not by mineralocorticoid receptor antagonism, suggesting a glucocorticoid receptor-mediated pathway. The intravenous prednisolone suppression test provides a powerful new tool to investigate HPA abnormalities underlying metabolic and psychiatric disease states.

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Section: Discussionsupporting

confidence: 84%

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

Russell¹,

Henley²,

Leendertz³

et al. 2010

J. Neurosci.

106

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“…ATI is the protein synthesis inhibitor, which could block the protein synthesis by genomic mechanism pathway [8,26,28]. The sensitized cells were preincubated with ATI (10 -4 M) for 3 h, and then incubated with HG (10 -7 M) for 7 min before antigen added.…”

Section: Non-genomic Effects Of Hg On Histamine Release From Mast Cellsmentioning

confidence: 99%

A novel strategy for development of glucocorticoids through non-genomic mechanism

Zhou

Sheng

et al. 2010

Cell. Mol. Life Sci.

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Glucocorticoids (GCs) are routinely believed to take effect through genomic mechanisms, which are also largely responsible for GCs' side effects. Beneficial non-genomic effects of GCs have been reported as being independent of the genomic pathway. Here, we synthesized a new type of GCs, which took effect mainly via non-genomic mechanisms. Hydrocortisone was conjugated with glycine, lysine and phenylalanine to get a bigger molecular structure, which could hardly go through the cell membrane. Evaluation of the anti-inflammatory efficacy showed that hydrocortisone-conjugated glycine (HG) and lysine could inhibit neutrophil degranulation within 15 min. HG could inhibit IgE-mediated histamine release from mast cells via a non-genomic pathway, and rapidly alleviate allergic reaction. Luciferase reporter assay showed that HG would not activate the glucocorticoid response element within 30 min, which verified the rapid effects independent of the genomic pathway. The work proposes a novel insight into the development of novel GCs, and provides new tools for experimental study on non-genomic mechanisms.

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“…Signaling by GR can be complicated, involving multiple receptor subtypes and both genomic and nongenomic actions. Rapid glucocorticoid effects generally involve cytosolic GRs, although GRs can also act within membranes to exert multiple rapid effects on various tissues and cells, as described in teleost and higher vertebrates (Borski, 2000;Roy and Rai, 2009). More specifically, membranebound GRs were found to have analogous ligand binding domains (epitope recognition, ligand specificity, and phosphorylation site) comparable with cytosolic GRs (Gametchu et al, 1999;Bartholome et al, 2004), and RU486 does not discriminate between the GR subtypes (Borski, 2000).…”

mentioning

confidence: 99%

Rapid, Nongenomic Stimulation of Multidrug Resistance Protein 2 (Mrp2) Activity by Glucocorticoids in Renal Proximal Tubule

Prevoo

Miller²,

Water³

et al. 2011

J Pharmacol Exp Ther

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In renal proximal tubule, multidrug resistance protein 2 (Mrp2) actively transports many organic anions into urine, including drugs and metabolic wastes. Upon exposure to nephrotoxicants or during endotoxemia, both Mrp2 activity and expression are up-regulated. This may result from induced de novo synthesis of Mrp2 or post-transcriptional events involving specific signaling pathways. Here, we investigated glucocorticoid signaling to Mrp2 in killifish renal proximal tubules, a model system in which transport activity can be measured using a fluorescent substrate and confocal imaging. Exposure of tubules to dexamethasone rapidly increased Mrp2-mediated fluorescein methotrexate transport. Other glucocorticoid receptor (GR) ligands, cortisol and triamcinolone acetonide, also stimulated Mrp2-mediated transport. The GR antagonist, mifepristone 17␤-hydroxy-11␤-[4-dimethylamino phenyl]-17␣-[1-propynyl] estra-4,9-dien-3-one (RU486), abolished stimulation by all three ligands, whereas the mineralocorticoid receptor antagonist, spironolactone, was ineffective. Consistent with action through a nongenomic mechanism, dexamethasone stimulation of Mrp2-mediated transport was insensitive to cycloheximide and actinomycin D, and immunohistochemistry revealed no alterations in Mrp2 expression at the luminal membrane. (9S-(9␣,10␤,12␣))-2,3,9,10,11,12-hexahydro-10-hydroxy-10-(methoxycarbonyl)-9-methyl-9,12-epoxy-1H-diindolo[1,2,3-fg:3Ј,2Ј,1Ј-kl]pyrrolo[3,4-i][1,6]benzodiazocin-1-one (K252a), an inhibitor of the tyrosine receptor kinase subfamily, reduced the dexamethasone effect, as did the specific hepatocyte growth factor receptor (c-Met) tyrosine kinase inhibitor, -665752). Hepatocyte growth factor (HGF), an endogenous ligand for c-Met, stimulated Mrp2-mediated transport. This effect was reversed by PHA-665752 but not by RU486. Inhibition of mitogenactivated protein kinase/extracellular signal-regulated kinase kinase (MEK 1/2) also abolished the effects of dexamethasone and HGF. Our results disclose a novel mechanism by which glucocorticoids acting through GR, c-Met, and MEK1/2 cause rapid, nongenomic stimulation of Mrp2-mediated transport in renal proximal tubules. This up-regulation may be nephroprotective, enhancing efflux of metabolic wastes and toxicants during cell and tissue stress.

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Genomic and non-genomic effect of cortisol on phagocytosis in freshwater teleost Channa punctatus: An in vitro study

Cited by 33 publications

References 36 publications

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

Rapid Glucocorticoid Receptor-Mediated Inhibition of Hypothalamic–Pituitary–Adrenal Ultradian Activity in Healthy Males

A novel strategy for development of glucocorticoids through non-genomic mechanism

Rapid, Nongenomic Stimulation of Multidrug Resistance Protein 2 (Mrp2) Activity by Glucocorticoids in Renal Proximal Tubule

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