Disease relevance of NO

• These effects of CPEE, coupled with increased glutamate release and increased NMDA receptor expression, may predispose the near-term foetal hippocampus to GR and Glu-NMDA receptor-mediated neurodevelopmental toxicity [1].
• As a first step toward elucidating the mechanism underlying the therapeutic effect of glucocorticoids on acute noise-induced hearing loss, we used semiquantitative reverse transcription polymerase chain reaction to study the level of glucocorticoid receptor (GR) mRNA in the cochlea of the guinea pig after acoustic overstimulation [2].
• Effect of saiboku-to (TJ-96) on bronchial asthma. Induction of glucocorticoid receptor, beta-adrenaline receptor, IgE-Fc epsilon receptor expression and its effect on experimental immediate and late asthmatic reaction [3].

Psychiatry related information on NO

• Changes in glucocorticoid receptor (GR) binding in different brain areas were investigated in neonatal and adult pigs exposed to psychological stress (weaning) and a physical stressor (repeated snaring) [4].

High impact information on NO

• Whole-cell binding assays were also performed, which resulted in similar quantities of maximally bound glucocorticoid receptor as well as the specificity of binding of various hormone analogs as found in the cytosol receptor assays [5].
• Dexamethasone response curves for these constructs show that the cortisol resistance observed in the guinea pig in vivo is conferred in vitro by the guinea pig GR LBD [6].
• Unique sequences in the guinea pig glucocorticoid receptor induce constitutive transactivation and decrease steroid sensitivity [6].
• One of the amino acid substitutions results in the loss of a cysteine, which in the human, rat, and mouse GR is the site of covalent attachment for dexamethasone-21-mesylate [6].
• The guinea pig GR has been cloned, and sequencing has identified many unique amino acid substitutions in the LBD [6].

Biological context of NO

• The phosphatase inhibitor, okadaic acid, and the protein kinase G activator, sodium nitroprusside, stimulate only GR-mediated transactivation, in contrast to modulators of other protein kinase pathways that act in parallel on both receptors [7].
• In female offspring (at estrus), glucocorticoid receptor mRNA levels were lower in the paraventricular nucleus and pars distalis but higher in the hippocampus in animals exposed to dexamethasone in utero [8].
• Since approximately 10% of pregnant women are treated with synthetic glucocorticoids in late gestation, to promote fetal organ maturation, we tested the hypothesis that fetal exposure to glucocorticoids modifies developing GR and MR systems in the brain [9].
• Hybridomas were screened for anti-GR antibody production by using an enzyme-linked immunosorbent assay [10].
• Furthermore, preincubation of the purified activated GR complex with 3A6 prevented phosphorylation of the GR in vitro [10].

Anatomical context of NO

• These data demonstrate that CPEE increases high glucocorticoid concentration-induced Glu release in the foetal hippocampus, presumably as a consequence of increased GR expression [1].
• GR, but not MR, mRNA expression was elevated in the hippocampus and dentate gyrus, whereas NR1 mRNA expression was increased in the CA1 and CA3 fields of the foetal hippocampus [1].
• Comparison of the interaction between the thyroid receptor and the GR, or the MR, distinguish two types of repression, only one of which is receptor-specific [7].
• There was no effect of dex on GR or MR mRNA in the male fetuses [9].
• Mineralocorticoid receptor mRNA in the limbic system and GR mRNA levels in the pars distalis were unaffected [11].

Associations of NO with chemical compounds

• Basal and electrically stimulated Glu and gamma-aminobutyric acid (GABA) efflux in the presence or absence of dexamethasone (DEX), a selective glucocorticoid-receptor agonist, were determined ex vivo in foetal hippocampal slices [1].
• 11beta-HSD type 1 (11beta-HSD-1) functions as a reductase in vivo, regulating intracellular cortisol levels and its access to the glucocorticoid receptor [12].
• We conclude that synthetic and endogenous glucocorticoids, as well as serotonin, can influence neuronal levels of GR mRNA during hippocampal development [13].
• Four days exposure to dexamethasone or corticosterone (10 or 100 nM) decreased levels of GR mRNA within neurons [13].
• Cytosol glucocorticoid receptor measurements were obtained by hydroxylapatite assay or column chromatography using Sephadex G-25 [5].

Other interactions of NO

• Our study shows conclusively that transport stress had long-term effects on cortisol, CBG and glucocorticoid receptor concentrations [14].
• Furthermore, the significant increase of TNF-alpha in the spleen caused by LPS was associated with a dramatic decrease in glucocorticoid receptor (GR) binding [15].

Analytical, diagnostic and therapeutic context of NO

• Differences in amounts of 11beta-HSD1, 11beta-HSD2, GR and MR mRNA were determined by quantitative real-time RT-PCR and data subjected to multivariate linear mixed model analysis [16].
• Immunocytochemical localization of the GR was assessed by indirect immunofluorescence in intact fixed cells, which demonstrated intense cytoplasmic staining in the absence of pretreatment with glucocorticoids and nuclear localization when cells were pretreated with glucocorticoids [10].
• In order to identify the nature of the glucocorticoid receptor (GR)-expressing neurons and pituitary cells that potentially mediate the negative effects of stress on reproductive performance, double immunohistochemical stainings were performed in the brain and pituitary of the rainbow trout (Oncorhynchus mykiss) [17].
• In the presence of serum, DNA synthesis was significantly inhibited by 50-63% when treated with 100 nM DXM, which was prevented by the glucocorticoid-receptor antagonist Org34116. mRNA levels of IGF axis components were determined using Northern blot analysis [18].
• To determine where in the cochlea the changes in glucocorticoid receptor mRNA levels occur, in situ hybridization histochemistry was performed with digoxigenin-labeled sense and antisense RNA probes complementary to guinea pig glucocorticoid receptor mRNA [2].

References