General Presence of Glucocorticoid Receptors in Mammalian Tissues<sup>1</sup>

Ballard, Philip L.; Baxter, John D.; Higgins, Stephen J.; Rousseau, Guy; Tomkins, Gordon M.

doi:10.1210/endo-94-4-998

Cited by 272 publications

(69 citation statements)

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“…As with liver, this last peak was mostly lost with 0-0.2 M NaC1 gradient (fig.2B); it is conclusive that an aldosterone binding component elutes at 0.06 M NaC1 from kidney cytosol which could not be revealed by either aldosterone in the liver ( fig.lD) or corticosterone in the kidney (fig.2D). This clear distinction between the steroid-specific receptors was lost when 0-1 M NaCI gradient was used, in keeping with the known tendency to disaggregate with high salt [6,11] and resulting in comparable elution proFdes in the liver and the kidney. The fact that no radioactivity could be eluted in the 0.001 M prewash when kidney cytosol was equilibrated with 10 -8 M corticosterone ( fig.2D), in place of aldosterone, constitutes a formal proof that, when observed, the same does not represent an artifact of the washing procedure.…”

Section: Methodsmentioning

confidence: 69%

“…These molecular sizes are comparable to those of corticosterone [4][5][6], the 'G' [2] or the steroid II [3] receptors, although neither peak corresponds to serum transcortin (62-63 000 daltons). The close similarity in molecular sizes, and the fact that transcortin is present to variable extent in most tissue preparations, obviate the importance of filtration through Sephadex gels; these are also true of sucrose density gradients further unsuitable due to huge dissociation during the lengthy centrifugation period [4][5][6]11 ].…”

Section: Methodsmentioning

confidence: 99%

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Demonstration of steroid specific hormone receptors by chromatography

Agarwal

1976

FEBS Letters

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Section: Methodsmentioning

confidence: 69%

Section: Methodsmentioning

confidence: 99%

Demonstration of steroid specific hormone receptors by chromatography

Agarwal

1976

FEBS Letters

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“…Only a few studies concern the presence of GR in bronchial cells, and the majority used animal studies [26][27][28][29]. Previous in vitro binding experiments with 3 H-dexamethasone performed on lung samples from adult and foetal animals and from a human foetus showed nuclear localization of 3 H-dexamethasone in alveolar epithelial cells, but no significant nuclear localization in bronchial epithelial cells [26][27][28][29]. In these studies autoradiographic data were confirmed with liquid scintillation counting for specific 3 H-dexamethasone binding in nuclear and cytosolic fractions prepared from lung tissue.…”

Section: Discussionmentioning

confidence: 99%

Modulation of glucocorticoid receptor expression in human bronchial epithelial cell lines by IL-1 beta, TNF-alpha and LPS

Verheggen¹,

Hal²,

Adriaansen-Soeting³

et al. 1996

Eur Respir J

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M Mo od du ul la at ti io on n o of f g gl lu uc co oc co or rt ti ic co oi id d r re ec ce ep pt to or r e ex xp pr re es ss si io on n i in n h hu um ma an n b br ro on nc ch hi ia al l e ep pi it th he el li ia al l c ce el ll l l li in ne es s b by y I IL L--1 1β, , T TN NF F--α a an nd d L LP PS S nM, respectively. Using electrophoretic mobility shift assays we demonstrated the binding of nuclear translocated GR to specific sites on deoxyribonucleic acid (DNA), named glucocorticoid responsive elements (GRE).Lipopolysaccharide (LPS) and interleukin-1β (IL-1β) significantly increased the number of GR per cell (median=312% and 171% of control, respectively; p<0.05), but significantly reduced the ligand affinity of these receptors, i.e. increased the Kd (median=410% and 145% of control, respectively; p<0.05) in BEAS 2B cells.These results indicate that the bronchial epithelium may be an actual target for glucocorticoid therapy. Inflammatory mediators, such as IL-1β and LPS, modulate the number and ligand affinity of these GR. Therefore, the response of bronchial epithelium to glucocorticoid therapy may be modulated by airway diseases associated with inflammation. Eur Respir J., 1996Respir J., , 9, 2036Respir J., -2043

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“…The appearance in specific embryonic tissues of cytoplasmic glucocorticoid receptors at discrete developmental stages has been implicated as one factor that determines the appearance of hormonal responsiveness in these tissues (25). Likewise, the presence of functional nuclear acceptor proteins for the steroid-receptor complex is also required for embryonic target tissues about to undergo hormone-dependent differentiation (26,27).…”

Section: Glucocorticoid-induced Cleft Palatementioning

confidence: 99%

Receptor-Dependent Mechanisms of Glucocorticoid and Dioxin-Induced Cleft Palate

Pratt¹

1985

Environmental Health Perspectives

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Glucocorticoids (triamcinolone) and dioxins (TCDD) are highly specific teratogens in the mouse, in that cleft palate is the major malformation observed. Glucocorticoids and TCDD both readily cross the yolk sac and placenta and appear in the developing secondary palate. Structure-activity relationships for glucocorticoid-and TCDD-induced cleft palate suggest a receptor involvement. Receptors for glucocorticoids and TCDD are present in the palate and their levels in various mouse strains are highly correlated with their sensitivity to cleft palate induction. Receptors for glucocorticoids appear to be more prevalent in the palatal mesenchymal cells whereas those for TCDD are probably located in the palatal epithelial cells. Glucocorticoids exert their teratogenic effect on the palate by inhibiting the growth of the palatal mesenchymal cells whereas TCDD alters the terminal cell differentiation of the medial palatal epithelial cells. Glucocorticoid-Induced Cleft PalateGlucocorticoids administered to several species of experimental animals at midgestation inhibit complete formation of the secondary palate (1-4). Development of the mammalian secondary palate is a complex process that depends upon the presence of various hormones and growth factors (5). The palatal shelves first appear as outgrowths from the maxillary process and subsequently grow in a vertical position alongside the tongue. The shelves undergo a rapid reorientation to the horizontal position above the tongue which brings the apposing epithelia into contact at the midline. The medial epithelial cells then undergo a programmed cell death with resorption ofthe basement membrane and cell remnants, and the two shelves fuse into a single tissue, the secondary palate, which separates the oral and nasal cavities (6,7).Different strains of inbred mice exhibit different degrees of susceptibility to glucocorticoid-induced cleft palate (1,8 (5,11,12). Walker and Fraser (6) showed that during normal development, the palatal shelves became horizontal later in the A/J than the C57BL/6J strain and suggested that this difference makes A/J mice more susceptible to cortisone than C57BL/6J mice (13). A recent study utilizing frozen sections (14) showed that, in addition to delaying palatal shelf elevation, cortisone treatment severely reduced the extent of contact between the palatal shelves in A/J mice. Although contact was present in 20% of the cortisone-treated fetuses, the mean area of the shelf contact was only 20% of that in control palates. Therefore, the net shelf contact in cortisone-treated litters was only 4% of the potential contact in control litters. Other studies in which shelf contact was assessed in glucocorticoid-treated fetuses reported contact in 27-30% of the fetuses. However, this limited contact, observed between the shelves in the midpalate region, was considered adequate for complete palatal fusion, and a failure in the fusion mechanism was proposed as an alternative (4,15). Diewert and Pratt (14) also observed shelf contact in the midpalate re...

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General Presence of Glucocorticoid Receptors in Mammalian Tissues¹

Cited by 272 publications

References 0 publications

Demonstration of steroid specific hormone receptors by chromatography

Demonstration of steroid specific hormone receptors by chromatography

Modulation of glucocorticoid receptor expression in human bronchial epithelial cell lines by IL-1 beta, TNF-alpha and LPS

Receptor-Dependent Mechanisms of Glucocorticoid and Dioxin-Induced Cleft Palate

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General Presence of Glucocorticoid Receptors in Mammalian Tissues1

Cited by 272 publications

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Demonstration of steroid specific hormone receptors by chromatography

Demonstration of steroid specific hormone receptors by chromatography

Modulation of glucocorticoid receptor expression in human bronchial epithelial cell lines by IL-1 beta, TNF-alpha and LPS

Receptor-Dependent Mechanisms of Glucocorticoid and Dioxin-Induced Cleft Palate

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General Presence of Glucocorticoid Receptors in Mammalian Tissues¹