The antiglucocorticoid action of mifepristone

Agarwal, M.K.

doi:10.1016/0163-7258(96)00016-2

Cited by 59 publications

(40 citation statements)

References 345 publications

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“…This assumption was supported by the fact that gluco-and mineralocorticoids cross react easily 4,5 and glucocorticoid action is intimately linked to the physiopathology of hematopoietic cells. 6,16 Consequently, we explored the possible presence of the MCR and of the ASSC in various types of hematopoietic cells, including the human leukemic cell lines.…”

Section: Introductionmentioning

confidence: 67%

“…Cells were exposed for 18 h to 1% ethanol alone (1) or steroids dissolved in ethanol (1% final) as follows: 10 M aldosterone (2), 3 or 0.3 M ZK 91587 (3,4), and aldosterone plus ZK 91587 (5,6). The cultures were thereafter treated with 200 l Hoechst 33342 for 30 min in the dark, and processed for fluorescence as described in the Methods section.…”

Section: Figure 10mentioning

confidence: 99%

“…11,12 Corticotherapy is also associated with a number of sideeffects. 4,5 Little information is currently available regarding the possible presence of the mineraloreceptor (MCR) and of their physiological effect on hematopoietic cells. Thus, lymphocytes are endowed with the MCR although its functional relevance there remains unknown.…”

Section: Introductionmentioning

confidence: 99%

“…The steroid molecule binds to appropriate high affinity, low capacity soluble receptor(s) that recognizes the cognate hormone response element (HRE) in the proximal promoter via two zinc fingers for the transactivation of specific genes, that are cell and tissue-dependent. [1][2][3][4][5] Whereas the mechanism of action of glucocorticoids has been extensively studied, relatively little information is available regarding mineralocorticoids.…”

Section: Introductionmentioning

confidence: 99%

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Demonstration of the mineralocorticoid hormone receptor and action in human leukemic cell lines

Mirshahi

Golestaneh

et al. 2000

Leukemia

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We studied the expression of the mineralocorticoid receptor (MCR), and of the amiloride-sensitive sodium channel (ASSC) regulated by the MCR, in human leukemic cell lines. Cell extracts from TF1 (proerythroblastic), HEL (human erythroblastic leukemia) and U937 (myeloblastic) cell line were positive for the ASSC, as a 82 kDa band in Western blots developed with the aid of a polyclonal antibody raised against the peptide QGLGKGDKREEQGL, corresponding to the region 44-58 of the ␣ subunit of the epithelial sodium channel (ENaC) cloned from rat colon, linked to KLH. The polyclonal antibody against the MCR revealed a single band of about 102 kDa in extracts from HEL and TF1 cells. The immunofluorescent labelling of the MCR in all cell lines showed a nucleocytoplasmic localization of the receptor but the ASSC was exclusively membrane-bound and these results were confirmed by confocal microscopy. The expression of the MCR in the HEL cells was evident as a predicted band of 843 bp (234 amino acids) in electrophoresis of the PCR product obtained after total RNA had been reverse transcribed and then amplified using the primers 5′-AGGCTAC-CACAGTCTCCCTG-3′ and 5′-GCAGTGTAAAATCTCCAGTC-3′ (sense and antisense, respectively). The ENaC was similarly evident with the aid of the primers 5′-CTGCCTTTATG GATGATGGT-3′ (sense) and 5′-GTTCAGCTCGAAGAAGA-3′ (antisense) as a predicted band of 520 bp. In both cases, 100% identity was observed between the sequences of the PCR products compared to those from known human sources. The multiplication of the HEL cells was influenced by antagonists (RU 26752, ZK 91587) targeted for specificity to the MCR and this was selectively reversed by the natural hormone aldosterone. These steroids also provoked chromatin condensation in the HEL population. These permit new and novel possibilities to understand the pathobiology of human leukemia and to delineate sodium-water homeostasis in nonepithelial cells. Leukemia (2000) 14, 1097-1104.

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Section: Introductionmentioning

confidence: 67%

Section: Figure 10mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Demonstration of the mineralocorticoid hormone receptor and action in human leukemic cell lines

Mirshahi

Golestaneh

et al. 2000

Leukemia

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“…In contrast, aldosterone did not inhibit [ 3 H]thymidine incorporation by Ox-LDL (Figure 2). Moreover, other steroids, including To investigate whether transactivation of glucocorticoid receptor by dexamethasone causes inhibition of Ox-LDLinduced macrophage growth, we examined the effect of RU-486, a glucocorticoid receptor antagonist, 33 on this phenomenon. As shown in Figure 3, [ 3 H]thymidine incorporation into macrophages was not affected by RU-486 in the presence or absence of Ox-LDL.…”

Section: Glucocorticoids Inhibit Ox-ldl-induced Macrophage Growthmentioning

confidence: 99%

Glucocorticoid Inhibits Oxidized LDL-Induced Macrophage Growth by Suppressing the Expression of Granulocyte/Macrophage Colony-Stimulating Factor

Sakai

Biwa

Matsumura

et al. 1999

ATVB

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Abstract-Glucocorticoid, an anti-inflammatory agent, inhibits the development of atherosclerosis in various experimental animal models. This is partially explained by its ability to inhibit smooth muscle cell migration and proliferation in the intima and to reduce chemotaxis of circulating monocytes and leukocytes into the subendothelial spaces. We have recently demonstrated that oxidized LDL (Ox-LDL) has a mitogenic activity for macrophages in vitro in which Ox-LDL-induced granulocyte/macrophage colony-stimulating factor (GM-CSF) production plays an important role. Proliferation of cellular components is one of the characteristic events in the development and progression of atherosclerotic lesions. In the present study, we investigated the effects of glucocorticoids on Ox-LDL-induced macrophage growth. Dexamethasone, prednisolone, and cortisol inhibited Ox-LDL-induced thymidine incorporation into macrophages by 85%, 70%, and 50%, respectively. Ox-LDL induced a significant production of GM-CSF by macrophages, which was effectively inhibited by dexamethasone, prednisolone, and cortisol by 80%, 65%, and 50%, respectively. Dexamethasone-mediated inhibition of Ox-LDL-induced GM-CSF mRNA expression and macrophage growth was significantly abrogated by RU-486, a glucocorticoid receptor antagonist. Our results suggest that the inhibitory effects of glucocorticoids on macrophage growth may be due to the inhibition of Ox-LDL-induced GM-CSF production through transactivation of the glucocorticoid receptor. (Arterioscler Thromb Vasc Biol.

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Hormones, 1. Hormone Systems

Sandow¹

2011

Ullmann's Encyclopedia of Industrial Chemistry

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The article contains sections titled: 1. Introduction 1.1. Definitions and Classification 1.2. Hormone‐Producing Systems 1.3. Structural Analysis and Synthesis 1.4. Receptors and Mechanisms of Action 1.5. Therapeutic Use of Hormones 2. Peptide and Protein Hormones 2.1. Hypothalamic Hormones 2.2. Proopiomelanocortin Hormones 2.3. Glycoprotein Hormones 2.4. Growth Hormone, Prolactin, and Placental Lactogen 2.5. Calcium‐Regulating Hormones 2.6. Glucose‐Regulating Hormones 2.7. Gastrointestinal Hormones 2.8. Growth Factors and Related Peptides 2.9. Cardiovascular Hormones 3. Amino Acid Derivatives 3.1. Catecholamines and Indolamines 3.2. Thyroid Hormones 3.3. Thyromimetics 4. Steroid Hormones 4.1. Estrogens, Gestagens 4.2. Androgens 4.3. Adrenal Steroids 5. Prostaglandins 6. Hormone Analogs and Antagonists

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The antiglucocorticoid action of mifepristone

Cited by 59 publications

References 345 publications

Demonstration of the mineralocorticoid hormone receptor and action in human leukemic cell lines

Demonstration of the mineralocorticoid hormone receptor and action in human leukemic cell lines

Glucocorticoid Inhibits Oxidized LDL-Induced Macrophage Growth by Suppressing the Expression of Granulocyte/Macrophage Colony-Stimulating Factor

Hormones, 1. Hormone Systems

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