Disease relevance of Dectancyl

• The effects of NIM and DEX on transcriptional activation of the mouse mammary tumor virus (MMTV) promoter was determined by transfecting HSF with MMTV-luciferase (reporter gene) constructs [1].
• Here, we show that treatment of H4IIE hepatoma cells with the synthetic glucocorticoid, dexamethasone (dex), induces the accumulation of glucocorticoid receptor, as well as many transcription factors, coregulators, and RNA polymerase II, on the PEPCK gene promoter [2].
• From merely a cost/benefit ratio, the evaluation of DHEA-S levels and dex suppression has sufficient sensitivity to identify the occurrence of silent hypercortisolism [3].
• Two glucocorticoid receptor-containing clones of human acute lymphoblastic leukemia, one (CEM-C7) sensitive and one (CEM-C1) resistant to dexamethasone (dex) were studied in an effort to identify the time course of the biochemical changes responsible for dex-induced growth inhibition of CEM-C7 cells [4].
• Acute dexamethasone (Dxmn, 30 microg/kg body weight, i.v.) treatment induced a very rapid decrease in plasma ACTH concentrations in both Sham and ADX rats, as well as a decrease in plasma B levels in Sham rats [5].

Psychiatry related information on Dectancyl

• CONCLUSIONS: The dex/CRH test is abnormal in both remitted and non-remitted patients with bipolar disorder [6].
• In a first series of studies a refined neuroendocrine test to probe the integrity of HPA system status--the combined dexamethasone suppression/CRH challenge (DEX/CRH) test--was developed and the differential effects of aging and depressed psychopathology on DEX/CRH test outcome were described [7].

High impact information on Dectancyl

• Similarly, PGI2 synthesis from arachidonic acid fell 86% with DEX; all of the above effects are consistent with COX-1 downregulation [8].
• We therefore studied the direct effects of dexamethasone (DEX) on COX-1 expression in early-passage ovine fetal pulmonary-artery endothelial cells (PAECs) [8].
• DEX (10(-10) to 10(-6) mol/L) caused a dose-related decrease in COX-1 mRNA expression that was evident by 24 hours, was maximal at 10(-6) mol/L (50% inhibition), and was not due to changes in mRNA stability [8].
• In adult rats, hypophysectomy prevented the rise in PRS due to EE2 but did not prevent the increase in PRS due to Dex [9].
• DEX increased cellular metallothionein content by 1.6-fold in NIH 3T3 cells and 3.3-fold in LTR H-ras(A) cells [10].

Chemical compound and disease context of Dectancyl

• RESULTS: Patients with bipolar disorder demonstrated an enhanced cortisol response to the dex/CRH test compared with controls (P=0.001) [6].
• Pretreatment of the rats with dexamethasone (DEX) prevented the hypotension, attenuated the increase in plasma NOx and biopterin concentrations, and significantly inhibited the increase in lung biopterin content caused by LPS treatment [11].
• Suppression of P release by injection of dexamethazone or corticosterone or by adrenalectomy resulted in testicular hemorrhage and production of only metalicthionein after Cd exposure [12].
• The degree of VD2 toxicity, enhanced by DEX, was correlated with the degree of hypercalcemia and tissue calcification [13].
• DEX pretreatment (25muM, 48h) significantly increased CYP3A7-catalyzed luciferin 6' benzylether O-debenzylation, but had no effect on alachlor toxicity [14].

Biological context of Dectancyl

• Together, these data support the hypothesis that resistance to Dxm-induced apoptosis in NOD immature thymocytes is controlled by a genetic factor within the region that also contributes to type 1 diabetes pathogenesis [15].
• Herein, we refine this phenotype using a time-course experiment of apoptosis induction upon Dxm treatment [15].
• RESULTS: NIM had no effect on the number of GR binding sites, in contrast to NAP and DEX [1].
• Extent of the expression of neuron-associated properties in several cell clones after the addition of dexamethazone (DEX) seems to correlate well with the levels of the v-Ha-ras gene expression [16].
• The inhibition of cellular proliferation which occurs at 48 h after release in the dex-treated CEM-C7 cells was preceded by an inhibition of acetate incorporation into cholesterol, first evident at 24 h, inhibition of protein synthesis at 30 h, and the development of a cell cycle block in G1 at 36 h [4].

Anatomical context of Dectancyl

• In nontransfected wild-type NIH 3T3 cells, DEX did not induce DDP resistance nor did it decrease DDP accumulation [10].
• After the induction of v-Ha-ras expression with DEX in these cell lines, sustained elevation of the levels of cAMP as well as of phosphatidylinositol (PtdIns) metabolites, inositol trisphosphate, and diacylglycerol, is observed [16].
• DEX treatment increased adrenal gland cholesteryl ester and oil red O staining in z. fasciculata cells in which the apoE mRNA concentration was increased as well as in other cortical cells in which apoE mRNA was unchanged [17].
• These cells accumulate lipids and differentiate into adipocytes when treated with insulin, triiodothyronine and dexamethazone [18].
• 3H-RU 486 binds with high affinity (KDeq approximately 0.4 nM) to the same high affinity receptor-binding sites as dex (KD approximately 0.5 nM) in the cell cytosol, as indicated by Scatchard plot, gradient-ultracentrifugation and competition studies [19].

Associations of Dectancyl with other chemical compounds

• Despite no difference in basal pituitary-adrenal activity or in their ACTH and cortisol responses to CRH, LBW men had significantly lower pituitary-adrenal responses in the DEX/CRH test [20].
• When HeLa cells were treated with both estradiol and Dex, the steroids counteracted each other's transcriptional effects [21].
• When administered in combination with RU486, dex partially reversed the increased uterine intraluminal fluid retention at 0900 h estrus, but did not modify the inhibitory effect of RU486 on the primary gonadotropin surges or the secondary surge of FSH [22].
• Moreover, the simultaneous injection of DEX and progesterone yielded an additive effect on the relative rates of ovalbumin and conalbumin gene transcription [23].
• The CRH part of the DEX/CRH-test outcome might indicate the loss of endogenous CRH-Arginine-Vasopressin (AVP) synergism of the HPA system of these patients [24].

Gene context of Dectancyl

• We have previously reported that resistance of NOD immature thymocytes to depletion by dexamethazone (Dxm) maps to the Idd6 locus [15].
• In addition, quantitative PCR shows that DEX down-regulates GR and up-regulates glucocorticoid-induced leucine zipper levels, whereas ICI 182,780 does not counteract these effects [25].
• The amount of transfected estrogen and glucocorticoid receptors (ER and GR) determined the extent to which Dex blunted estrogen stimulation or estrogen prevented Dex inhibition [21].
• On the other hand, expression of another secretagogue of ACTH, arginine vasopressin (AVP), was differently affected in the PVN parvocellular neurons of offspring of the DEX group since AVP mRNA increased whereas immunoreactive content of the PVN parvocellular neurons was lowered [26].
• ET-1 gene expression increases significantly, parallel to the increase in beta-casein gene expression, in epithelial cell lines (HC11) of mouse mammary gland after hormonal stimulation by addition of dexamethazone and prolactin [27].

Analytical, diagnostic and therapeutic context of Dectancyl

• In frozen sections, the GR immunoreactivity in cell nuclei was weak in the absence and very strong in the presence of Dex, while no GR-specific cytoplasmic staining was observed [28].
• Northern blot analysis showed marked blunting of mRNA expression in RMC treated with DX, in concordance with functional studies [29].
• Quantitative Western blot analysis and immunocytochemistry indicated that ACTH and 17alpha-E2 treatment greatly increased SR-BI expression in the adrenal (especially in the microvillar compartment of adrenocortical cells), whereas DEX treatment led to a decrease of SR-BI by all measurements [30].
• The inhibitory effect of DX was confirmed using a reporter cell bioassay, whereas cGMP was measured as a reflection of bioactive NO [29].
• Male Sprague-Dawley rats (3 or 24 mo old) were divided into seven groups: three groups received 1.5 mg/kg of DEX once a day by intraperitoneal injection for 3, 5, or 7 days; three groups were pair fed to the three treated groups, respectively; and one control group of healthy rats was fed ad libitum [31].

References