The Experts below are selected from a list of 168 Experts worldwide ranked by ideXlab platform
Melvyn S. Soloff - One of the best experts on this subject based on the ideXlab platform.
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Effectors of Cyclic Adenosine 5'-Monophosphate Up-Regulating-Oxytocin Receptors in Rabbit Amnion Cells: Isoproterenol, Parathyroid Hormone-Related Protein, and Potentiation by Cortisol'
2016Co-Authors: Yow-jiun Jeng, Er Hinko, Melvyn S. SoloffAbstract:Forskolin (FSK; an activator of adenylyl cyclase) and cortisol synergistically increase the concentration of oxytocin receptors (OTRs) in rabbit amnion cells. The aims of this study were to characterize potential physiological regulators of OTR concentrations acting through adenylyl cyclase and to clarify the mechanisms of potentiation by cAMP and cortisol. Both isoproterenol (ISO) and parathyroid hormone-related protein (PTHrP) elevated amnion cell cAMP levels and OTR concentrations. The effects of ISO and PTHrP on OTR were potentiated by cortisol. Cortisol had no effect on the ability of ISO or PTHrP to stimulate adenylyl cyclase activity, and cAMP did not affect the number or affinity of Glucocorticoid receptors in whole cells or in cytosol. Adenylyl cyclase activation, however, caused conversion of mifepristone (RU486) from a Glucocorticoid Antagonist to agonist. Thus, mifepristone elevated OTR receptor concentrations in the presence of FSK. In contrast, a structurally related Glucocorticoid Antagonist, onapristone (ZK98 299), was unaffected by cAMR Because Glucocorticoid recep-tors bound to mifepristone are capable of interacting with DNA, whereas onapristone-occupied receptors are not, we conclude that cAMP affects Glucocorticoid receptor-DNA interactions, accounting for the synergistic effects of cAMP and cortisol on OTRs
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Effectors of cyclic adenosine 5'-monophosphate up-regulating-oxytocin receptors in rabbit amnion cells: isoproterenol, parathyroid hormone-related protein, and potentiation by cortisol.
Biology of reproduction, 1995Co-Authors: Yow-jiun Jeng, Alexander Hinko, Melvyn S. SoloffAbstract:Forskolin (FSK ; an activator of adenylyl cyclase) and cortisol synergistically increase the concentration of oxytocin receptors (OTRs) in rabbit amnion cells. The aims of this study were to characterize potential physiological regulators of OTR concentrations acting through adenylyl cyclase and to clarify the mechanisms of potentiation by cAMP and cortisol. Both isoproterenol (ISO) and parathyroid hormone-related protein (PTHrP) elevated amnion cell cAMP levels and OTR concentrations. The effects of ISO and PTHrP on OTR were potentiated by cortisol. Cortisol had no effect on the ability of ISO or PTHrP to stimulate adenylyl cyclase activity, and cAMP did not affect the number or affinity of Glucocorticoid receptors in whole cells or in cytosol. Adenylyl cyclase activation, however, caused conversion of mifepristone (RU486) from a Glucocorticoid Antagonist to agonist. Thus, mifepristone elevated OTR receptor concentrations in the presence of FSK. In contrast, a structurally related Glucocorticoid Antagonist, onapristone (ZK98 299), was unaffected by cAMP. Because Glucocorticoid receptors bound to mifepristone are capable of interacting with DNA, whereas onapristone-occupied receptors are not, we conclude that cAMP affects Glucocorticoid receptor-DNA interactions, accounting for the synergistic effects of cAMP and cortisol on OTRs.
Tadashi Inagami - One of the best experts on this subject based on the ideXlab platform.
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steroid hormones upregulate rat angiotensin ii type 1a receptor gene role of Glucocorticoid responsive elements in rat angiotensin ii type 1a promoter
The Journal of Steroid Biochemistry and Molecular Biology, 1995Co-Authors: Tadashi InagamiAbstract:Abstract The transcription of the rat angiotensin II type 1A receptor gene is stimulated by Glucocorticoids. To clarify the molecular mechanism for Glucocorticoid action in rat vascular smooth muscle cells, we investigated the effects of dexamethasone on the promoter activity of the angiotensin II type 1A receptor by using promoter/luciferase reporter gene constructs and heterologous context constructs (containing the thymidine kinase promoter) in transfected vascular smooth muscle cells. There are three putative Glucocorticoid responsive elements in the promoter. However, only one Glucocorticoid responsive element was found to respond to dexamethasone (1 μM). The region was located at positions, −756 to −770 bp upstream of the transcription initiation site. A Glucocorticoid Antagonist, RU38486, completely blocked the induction by dexamethasone, suggesting that the Glucocorticoid responsive element was functional through a specific Glucocorticoid receptor. Compared with the angiotension II type 1A receptor promoter, no effect by dexamethasone was observed in vascular smooth muscle cells transfected with the angiotensin II type 1B receptor promoter/luciferase reporter gene constructs. We concluded that the dexamethasone-induced increase in the transcription of the angiotensin II type 1A receptor gene occurred through the binding to GRE up the Glucocorticoid-specific receptor.
Yow-jiun Jeng - One of the best experts on this subject based on the ideXlab platform.
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Effectors of Cyclic Adenosine 5'-Monophosphate Up-Regulating-Oxytocin Receptors in Rabbit Amnion Cells: Isoproterenol, Parathyroid Hormone-Related Protein, and Potentiation by Cortisol'
2016Co-Authors: Yow-jiun Jeng, Er Hinko, Melvyn S. SoloffAbstract:Forskolin (FSK; an activator of adenylyl cyclase) and cortisol synergistically increase the concentration of oxytocin receptors (OTRs) in rabbit amnion cells. The aims of this study were to characterize potential physiological regulators of OTR concentrations acting through adenylyl cyclase and to clarify the mechanisms of potentiation by cAMP and cortisol. Both isoproterenol (ISO) and parathyroid hormone-related protein (PTHrP) elevated amnion cell cAMP levels and OTR concentrations. The effects of ISO and PTHrP on OTR were potentiated by cortisol. Cortisol had no effect on the ability of ISO or PTHrP to stimulate adenylyl cyclase activity, and cAMP did not affect the number or affinity of Glucocorticoid receptors in whole cells or in cytosol. Adenylyl cyclase activation, however, caused conversion of mifepristone (RU486) from a Glucocorticoid Antagonist to agonist. Thus, mifepristone elevated OTR receptor concentrations in the presence of FSK. In contrast, a structurally related Glucocorticoid Antagonist, onapristone (ZK98 299), was unaffected by cAMR Because Glucocorticoid recep-tors bound to mifepristone are capable of interacting with DNA, whereas onapristone-occupied receptors are not, we conclude that cAMP affects Glucocorticoid receptor-DNA interactions, accounting for the synergistic effects of cAMP and cortisol on OTRs
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Effectors of cyclic adenosine 5'-monophosphate up-regulating-oxytocin receptors in rabbit amnion cells: isoproterenol, parathyroid hormone-related protein, and potentiation by cortisol.
Biology of reproduction, 1995Co-Authors: Yow-jiun Jeng, Alexander Hinko, Melvyn S. SoloffAbstract:Forskolin (FSK ; an activator of adenylyl cyclase) and cortisol synergistically increase the concentration of oxytocin receptors (OTRs) in rabbit amnion cells. The aims of this study were to characterize potential physiological regulators of OTR concentrations acting through adenylyl cyclase and to clarify the mechanisms of potentiation by cAMP and cortisol. Both isoproterenol (ISO) and parathyroid hormone-related protein (PTHrP) elevated amnion cell cAMP levels and OTR concentrations. The effects of ISO and PTHrP on OTR were potentiated by cortisol. Cortisol had no effect on the ability of ISO or PTHrP to stimulate adenylyl cyclase activity, and cAMP did not affect the number or affinity of Glucocorticoid receptors in whole cells or in cytosol. Adenylyl cyclase activation, however, caused conversion of mifepristone (RU486) from a Glucocorticoid Antagonist to agonist. Thus, mifepristone elevated OTR receptor concentrations in the presence of FSK. In contrast, a structurally related Glucocorticoid Antagonist, onapristone (ZK98 299), was unaffected by cAMP. Because Glucocorticoid receptors bound to mifepristone are capable of interacting with DNA, whereas onapristone-occupied receptors are not, we conclude that cAMP affects Glucocorticoid receptor-DNA interactions, accounting for the synergistic effects of cAMP and cortisol on OTRs.
Steven D Douglas - One of the best experts on this subject based on the ideXlab platform.
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the Glucocorticoid Antagonist ru 486 suppresses hiv infectivity and replication
Journal of Neuropsychiatry and Clinical Neurosciences, 2013Co-Authors: Tami D Benton, Kevin G Lynch, Benoit Dube, David R Gettes, Nancy B Tustin, Steven D Douglas, David S Metzger, Joshua Blume, Dwight L EvansAbstract:The effects of RU-486, a Glucocorticoid Antagonist, on HIV infection and replication in depressed and nondepressed women were studied using ex vivo models of HIV infection. RU-486 treatment of cells decreased HIV reverse transcriptase activity of monocyte-derived macrophages in a model of acute infectivity. RU-486 also decreased HIV viral replication in the chronically-infected T-cell line ACH-2, but not in the promonocyte cell line U1. No differences were associated with depression status. Thus, Glucocorticoid antagonism may suppress HIV infectivity and replication ex vivo. Studies to determine the role of Glucocorticoid Antagonists in the host defense against HIV should be performed.
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selective serotonin reuptake inhibitor and substance p Antagonist enhancement of natural killer cell innate immunity in human immunodeficiency virus acquired immunodeficiency syndrome
Biological Psychiatry, 2008Co-Authors: Dwight L Evans, Kevin G Lynch, Tami D Benton, Benoit Dube, David R Gettes, Nancy B Tustin, Jianping Lai, David Metzger, Steven D DouglasAbstract:Background Natural killer (NK) cells play an important role in innate immunity and are involved in the host defense against human immunodeficiency virus (HIV) infection. This study examines the potential role of three underlying regulatory systems that have been under investigation in central nervous system research as well as immune and viral research: serotonin, neurokinin, and Glucocorticoid systems. Methods Fifty-one HIV-seropositive subjects were recruited to achieve a representative sample of depressed and nondepressed women. The effects of a selective serotonin reuptake inhibitor (SSRI), a substance P (SP) Antagonist, and a Glucocorticoid Antagonist on NK cell function were assessed in a series of ex vivo experiments of peripheral blood mononuclear cells from each HIV-seropositive subject. Results Natural killer cell cytolytic activity was significantly increased by the SSRI citalopram and by the substance P Antagonist CP-96345 relative to control conditions; the Glucocorticoid Antagonist, RU486, showed no effect on NK cytotoxicity. Our results suggest that the effects of the three agents did not differ as a function of depression. Conclusions Our findings provide evidence that NK cell function in HIV infection may be enhanced by serotonin reuptake inhibition and by substance P antagonism. It remains to be determined if HIV-related impairment in not only NK cytolytic activity but also NK noncytolytic activity can be improved by an SSRI or an SP Antagonist. Clinical studies are warranted to address these questions and the potential roles of serotonergic agents and SP Antagonists in improving NK cell immunity, delaying HIV disease progression, and extending survival with HIV infection.
J W Funder - One of the best experts on this subject based on the ideXlab platform.
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high glucose stimulates aldosterone induced hypertrophy via type i mineralocorticoid receptors in neonatal rat cardiomyocytes
Endocrinology, 1996Co-Authors: A Sato, J W FunderAbstract:Previous studies have shown that aldosterone plus salt loading cause cardiac hypertrophy in rats in vivo, and that in vitro, both aldosterone and glucose stimulate fibroblast growth. The present studies examined the effects of adrenal steroids via mineralocorticoid and Glucocorticoid receptors (MR and GR) on [3H]leucine incorporation by neonatal rat cardiomyocytes in culture and the role of elevated glucose in modulating such effects. GR occupancy by corticosterone, the highly selective type II (Glucocorticoid) receptor agonist RU28362, or high doses of aldosterone lowers incorporation; when this effect is blocked by coincubation with the Glucocorticoid Antagonist RU486, aldosterone, but not corticosterone, markedly elevates leucine incorporation, indicating a specific mineralocorticoid effect via MR. Incubation with high glucose alone does not increase incorporation, but markedly increases the hypertropic effect of aldosterone in terms of both threshold and maximum response. The glucose-aldosterone syner...
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high glucose stimulates aldosterone induced hypertrophy via type i mineralocorticoid receptors in neonatal rat cardiomyocytes
Endocrinology, 1996Co-Authors: A Sato, J W FunderAbstract:Previous studies have shown that aldosterone plus salt loading cause cardiac hypertrophy in rats in vivo, and that in vitro, both aldosterone and glucose stimulate fibroblast growth. The present studies examined the effects of adrenal steroids via mineralocorticoid and Glucocorticoid receptors (MR and GR) on [3H]leucine incorporation by neonatal rat cardiomyocytes in culture and the role of elevated glucose in modulating such effects. GR occupancy by corticosterone, the highly selective type II (Glucocorticoid) receptor agonist RU28362, or high doses of aldosterone lowers incorporation; when this effect is blocked by coincubation with the Glucocorticoid Antagonist RU486, aldosterone, but not corticosterone, markedly elevates leucine incorporation, indicating a specific mineralocorticoid effect via MR. Incubation with high glucose alone does not increase incorporation, but markedly increases the hypertropic effect of aldosterone in terms of both threshold and maximum response. The glucose-aldosterone synergy is via MR and is completely blocked by spironolactone. The time course of increased incorporation is identical for aldosterone acting alone or with elevated glucose, consistent with widespread transcriptional effects and suggesting that the contribution of high glucose is not rate limiting. The glucose effect reflects neither induction of MR synthesis nor an increase in their affinity; it is specific, in that it is not mimicked by L-glucose or mannitol at equal concentrations, and is mediated via an increase in protein kinase C activity that can be measured in both soluble and particulate compartments. The role of this synergy in the cardiac sequelae of diabetes remains to be explored.