Retinoids modulate the binding capacity of the glucocorticoid receptor and its translocation from cytosol to nucleus in liver cells

Audouin-Chevallier, Isabelle; Pallet, Véronique; Coustaut, M.; Alfos, Serge; Higueret, Paul; Garcin, H

doi:10.1016/0960-0760(94)00184-n

Cited by 18 publications

(7 citation statements)

References 36 publications

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“…These data suggest that the increased iodide accumulation in MCF-7 cells after stimulation with atRA and Dex might be mediated by Dex-potentiated RAR/RXR heterodimerization and therefore increased ligand-dependent transcription of the NIS gene. In addition, Audouin-Chevallier et al (59) reported enhanced translocation of the glucocorticoid receptor from the cytosolic compartment to the nuclear compartment and stimulation of the binding capacity of glucocorticoid receptor after RA administration. This mechanism might further explain the additive effect of Dex and atRA in MCF-7 cells.…”

Section: Discussionmentioning

confidence: 96%

Dexamethasone Stimulation of Retinoic Acid-Induced Sodium Iodide Symporter Expression and Cytotoxicity of 131-I in Breast Cancer Cells

Unterholzner

Willhauck

Cengic

et al. 2006

The Journal of Clinical Endocrinology &Amp; Metabolism

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Section: Discussionmentioning

confidence: 96%

Dexamethasone Stimulation of Retinoic Acid-Induced Sodium Iodide Symporter Expression and Cytotoxicity of 131-I in Breast Cancer Cells

Unterholzner

Willhauck

Cengic

et al. 2006

The Journal of Clinical Endocrinology &Amp; Metabolism

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“…while retinoids have been found to alter the binding capacity of the glucocorticoid receptor and its translocation from the cytosol to the nucleus (Audouin-Chevallier et al 1995). Modulation of receptors might provide the basis for repression of resorption in the presence of both glucocorticoids and retinoids.…”

Section: Discussionmentioning

confidence: 99%

Differential effects of glucocorticoids on bone resorption in neonatal mouse calvariae stimulated by peptide and steroid-like hormones

Conaway¹,

Grigorie²,

Lerner³

1997

Journal of Endocrinology

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Differential effects on in vitro bone resorption were observed when the glucocorticoids, hydrocortisone and dexamethasone, were added to neonatal mouse calvariae treated with either parathyroid hormone (PTH), 1,25(OH)2-vitamin D3, all trans-retinoic acid (t-RA), or prostaglandin E2 (PGE2). Bone resorption was assessed by analyzing either the release of 45Ca from [45Ca]CaCl2 prelabeled calvarial bones or the release of 3H from [3H]proline prelabeled calvariae. At PGE2 concentrations of 3 x 10(-8) and 3 x 10(-7) mol/l, co-treatment with either 10(-6) mol/l dexamethasone or 10(-6) mol/l hydrocortisone caused additive 45Ca release from neonatal mouse calvariae. In contrast, synergistic release from mouse calvarial bones of both 45Ca and 3H was found after either 10(-6) mol/l hydrocortisone or 10(-6) mol/l dexamethasone was combined with 3 x 10(-11) mol/l PTH treatment for 120 h. Dose-response studies indicated that the synergistic stimulation of 45Ca release from neonatal mouse calvariae by glucocorticoids and PTH could be elicited at glucocorticoid concentrations of 10(-8) to 10(-6) mol/l and at PTH concentrations of 10(-11) to 10(-9) mol/l. Progesterone and RU 38486 (a derivative of 19-nortestosterone with antiglucocorticoid activity) blocked the synergism noted with glucocorticoid and PTH co-treatment, suggesting that interaction between the steroids and PTH was dependent on glucocorticoid receptor interaction. Addition of either 10(-6) mol/l hydrocortisone or 10(-6) mol/l dexamethasone to neonatal mouse calvariae treated with 1,25(OH)2-vitamin D3 (10(-11) and 10(-10) mol/l) also resulted in synergistic stimulation of 45Ca release. In contrast to these observations, the stimulatory effect of t-RA (10(-8) mol/l) on 45Ca release from calvarial bones was abolished in the presence of 10(-6) mol/l dexamethasone. These results suggest that an important role of glucocorticoids may be to synergistically potentiate bone resorption stimulated by PTH and 1,25(OH)2-vitamin D3, but indicate an opposing interaction between the glucocorticoids and bone resorptive retinoids.

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“…RA induces GR nuclear translocation, probably due to dissociation of GR from hsp90 in contrast with the ligand‐induced nuclear import. The effect of RA‐induced GR nuclear translocation on the function of the GR in the nucleus remains unknown . Other GR agonist‐like compounds, such as L‐carnitine (LCAR) and the pregnancy hormone relaxin, have been shown to induce GR activation by binding GR as a ligand and compete with dexamethasone (DEX) for binding to the GR LBD .…”

Section: Ligand‐induced Gr Nuclear Transportmentioning

confidence: 99%

On the Trail of the Glucocorticoid Receptor: Into the Nucleus and Back

Vandevyver

Dejager

Libert

2011

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146

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The glucocorticoid receptor (GR) belongs to the superfamily of steroid receptors and is an important regulator of physiological and metabolic processes. In its inactive state, GR is unbound by ligand and resides in the cytoplasm in a chaperone complex. When it binds glucocorticoids, it is activated and translocates to the nucleus, where it functions as a transcription factor. However, the subcellular localization of GR is determined by the balance between its rates of nuclear import and export. The mechanism of GR nuclear transport has been extensively studied. Originally, it was believed that nuclear import of GR is initiated by dissociation of the chaperone complex in the cytoplasm. However, several studies show that the chaperone machinery is required for nuclear transport of GR. In this review, we summarize the contribution of various chaperone components involved in the nuclear transport of GR and propose an updated model of its nuclear import and export. Moreover, we review the importance of ligand-independent nuclear transport and compare the nuclear transport of GR with that of other steroid receptors.

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Retinoids modulate the binding capacity of the glucocorticoid receptor and its translocation from cytosol to nucleus in liver cells

Cited by 18 publications

References 36 publications

Dexamethasone Stimulation of Retinoic Acid-Induced Sodium Iodide Symporter Expression and Cytotoxicity of 131-I in Breast Cancer Cells

Dexamethasone Stimulation of Retinoic Acid-Induced Sodium Iodide Symporter Expression and Cytotoxicity of 131-I in Breast Cancer Cells

Differential effects of glucocorticoids on bone resorption in neonatal mouse calvariae stimulated by peptide and steroid-like hormones

On the Trail of the Glucocorticoid Receptor: Into the Nucleus and Back

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