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Chemical Compound Review

AC1O5EDE     (9R,11S,16R)-9-fluoro-11,17- dihydroxy-17...

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Disease relevance of dexamethasone

  • Dexamethasone (Dex) stimulates the degradation of endogenous GR and p53 by the proteasome pathway in HUVEC under hypoxia and mitomycin C treatments, and also in hepatoma cells (HepG2) under normoxia [1].
  • Dexamethasone (DXM) (1 mg/kg per i.v.) given 1 h before or simultaneously with IC Hib LOS reduced significantly TNF activity and meningeal inflammation [2].
  • We conclude that DEX decreases both VDR number and mRNA in MG-63 osteosarcoma cells [3].
  • Treatment of 1-day-old rats for 4 days with 10 micrograms/day of the glucocorticoid dexamethasone (DEX) reduced IGF-II mRNA levels 10-fold in liver and inhibited body weight gain [4].
  • Enhancement of Ig production by DM and monocytes could be demonstrated with B cells obtained from a patient suffering from a hyperlymphocytic form of B cell type chronic lymphocytic leukemia, and in this case only IgM was produced [5].

Psychiatry related information on dexamethasone

  • OBJECTIVE: Studies using the dexamethasone suppression test (DST) have demonstrated an enhanced negative feedback inhibition at the pituitary in PTSD, but have not provided information about central feedback effects, since dexamethasone (DEX) does not penetrate the brain well [6].

High impact information on dexamethasone

  • We conclude that TNF participates in mediating meningeal inflammation associated with Hib experimental meningitis, and that DXM, when given before or with Hib LOS, inhibits CSF TNF production and modulates the meningeal inflammatory response [2].
  • Dox up-regulated the expression of the TRAIL receptor death receptor 5 (DR5) and synergistically enhanced the effect of TRAIL not only against MM cells sensitive to, but also against those resistant to, Dex- or Dox-induced apoptosis [7].
  • Dexamethasone (Dex), a synthetic glucocorticoid hormone, cooperated with Epo and stem cell factor to induce erythroid progenitors to undergo 15 to 22 cell divisions, corresponding to a 10(5)- to 10(6)-fold amplification of erythroid cells [8].
  • Dex acted directly on erythroid progenitors and maintained the colony-forming capacity of the progenitor cells expanded in liquid cultures [8].
  • This study showed the ability of the VIP-receptor (VIP-R) antagonist [N-Ac-Tyr1,D-Phe2]-GRF(1-29) amide to partially reverse the inhibitory effect of VIP and both PACAPs on DEX-induced apoptosis, providing evidence for a specific VIP1-R-mediated response and supporting the involvement of a single receptor for the three neuropeptides [9].

Chemical compound and disease context of dexamethasone


Biological context of dexamethasone


Anatomical context of dexamethasone


Associations of dexamethasone with other chemical compounds

  • STRO-1+ cells were cultured in the presence of dexamethasone (DEX; 10(-8) mol/L), ascorbic acid 2-phosphate (ASC-2P; 100 mumol/L), and inorganic phosphate (PO4i; 2.9 mmol/L) [21].
  • First, RU-486, which binds the glucocorticoid receptor and is a potent competitive antagonist of Dex, did not inhibit activation-induced cell killing [19].
  • Levels of c-fos and c-jun proteins also were increased by TNF alpha or ceramide in the presence of DEX [22].
  • DEX decreased VDR number (B max) by approximately 70% (110 versus 32 fmol/mg cellular protein, p less than 0.001) without significantly changing the apparent affinity (K'D) of 1,25-(OH)2D3 for its receptor (3.8 versus 2.2 x 10(-10) M, p greater than 0.05) [3].
  • The same subset is affected by dexamethasone (Dex); as reported for Dex-induced apoptosis, actinomycin D and cycloheximide also blocked Dox-induced apoptosis [23].

Gene context of dexamethasone


Analytical, diagnostic and therapeutic context of dexamethasone


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  4. Developmental and steroid hormonal regulation of insulin-like growth factor II expression. Levinovitz, A., Norstedt, G. Mol. Endocrinol. (1989) [Pubmed]
  5. B cell differentiation and interleukin 2 (IL2): corticosteroids interact with monocytes to enhance the effect of IL2. Emilie, D., Karray, S., Crevon, M.C., Vazquez, A., Galanaud, P. Eur. J. Immunol. (1987) [Pubmed]
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  7. TRAIL/Apo2L ligand selectively induces apoptosis and overcomes drug resistance in multiple myeloma: therapeutic applications. Mitsiades, C.S., Treon, S.P., Mitsiades, N., Shima, Y., Richardson, P., Schlossman, R., Hideshima, T., Anderson, K.C. Blood (2001) [Pubmed]
  8. The glucocorticoid receptor cooperates with the erythropoietin receptor and c-Kit to enhance and sustain proliferation of erythroid progenitors in vitro. von Lindern, M., Zauner, W., Mellitzer, G., Steinlein, P., Fritsch, G., Huber, K., Löwenberg, B., Beug, H. Blood (1999) [Pubmed]
  9. Vasoactive intestinal peptide and pituitary adenylate cyclase-activating polypeptides (PACAP27) and PACAP38) protect CD4+CD8+ thymocytes from glucocorticoid-induced apoptosis. Delgado, M., Garrido, E., Martinez, C., Leceta, J., Gomariz, R.P. Blood (1996) [Pubmed]
  10. Steroid hormonal independence of HER-2/neu mRNA expression in four human ovarian carcinoma cell lines. Jones, J., Lagasse, L.D., Karlan, B.Y. Gynecol. Oncol. (1994) [Pubmed]
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  13. BCL-2 expression in childhood leukemia versus spontaneous apoptosis, drug induced apoptosis, and in vitro drug resistance. Haarman, E.G., Kaspers, G.J., Pieters, R., van Zantwijk, C.H., Broekema, G.J., Hählen, K., Veerman, A.J. Adv. Exp. Med. Biol. (1999) [Pubmed]
  14. Functional properties of leptin receptor isoforms: internalization and degradation of leptin and ligand-induced receptor downregulation. Uotani, S., Bjørbaek, C., Tornøe, J., Flier, J.S. Diabetes (1999) [Pubmed]
  15. Distinct cytoplasmic domains of the growth hormone receptor are required for glucocorticoid- and phorbol ester-induced decreases in growth hormone (GH) binding. These domains are different from that reported for GH-induced receptor internalization. King, A.P., Tseng, M.J., Logsdon, C.D., Billestrup, N., Carter-Su, C. J. Biol. Chem. (1996) [Pubmed]
  16. Peroxisome proliferator-activated receptor alpha physically interacts with CCAAT/enhancer binding protein (C/EBPbeta) to inhibit C/EBPbeta-responsive alpha1-acid glycoprotein gene expression. Mouthiers, A., Baillet, A., Deloménie, C., Porquet, D., Mejdoubi-Charef, N. Mol. Endocrinol. (2005) [Pubmed]
  17. Analysis of chromatin structure of rat alpha1-acid glycoprotein gene; changes in DNase I hypersensitive sites after thyroid hormone, glucocorticoid hormone and turpentine oil treatment. Matsukawa, T., Kawasaki, H., Tanaka, M., Ohba, Y. Nucleic Acids Res. (1997) [Pubmed]
  18. Evidence for the involvement of distinct signal transduction pathways in the regulation of constitutive and interferon gamma-dependent gene expression of NADPH oxidase components (gp91-phox, p47-phox, and p22-phox) and high-affinity receptor for IgG (Fc gamma R-I) in human polymorphonuclear leukocytes. Amezaga, M.A., Bazzoni, F., Sorio, C., Rossi, F., Cassatella, M.A. Blood (1992) [Pubmed]
  19. Programmed T lymphocyte death. Cell activation- and steroid-induced pathways are mutually antagonistic. Zacharchuk, C.M., Merćep, M., Chakraborti, P.K., Simons, S.S., Ashwell, J.D. J. Immunol. (1990) [Pubmed]
  20. CD56+ cells induce steroid resistance in B cells exposed to IL-15. Xu, Q., Goleva, E., Ou, L.S., Li, L.B., Leung, D.Y. J. Immunol. (2004) [Pubmed]
  21. The STRO-1+ fraction of adult human bone marrow contains the osteogenic precursors. Gronthos, S., Graves, S.E., Ohta, S., Simmons, P.J. Blood (1994) [Pubmed]
  22. Tumor necrosis factor-alpha stimulates aromatase gene expression in human adipose stromal cells through use of an activating protein-1 binding site upstream of promoter 1.4. Zhao, Y., Nichols, J.E., Valdez, R., Mendelson, C.R., Simpson, E.R. Mol. Endocrinol. (1996) [Pubmed]
  23. Doxorubicin-induced DNA degradation in murine thymocytes. Zaleskis, G., Berleth, E., Verstovsek, S., Ehrke, M.J., Mihich, E. Mol. Pharmacol. (1994) [Pubmed]
  24. Apoptosis protection by the Epo target Bcl-X(L) allows factor-independent differentiation of primary erythroblasts. Dolznig, H., Habermann, B., Stangl, K., Deiner, E.M., Moriggl, R., Beug, H., Müllner, E.W. Curr. Biol. (2002) [Pubmed]
  25. Effects of glucocorticoids on tumor necrosis factor alpha-dependent activation of nuclear factor kappaB and expression of the intercellular adhesion molecule 1 gene in osteoblast-like ROS17/2.8 cells. Kurokouchi, K., Kambe, F., Kikumori, T., Sakai, T., Sarkar, D., Ishiguro, N., Iwata, H., Seo, H. J. Bone Miner. Res. (2000) [Pubmed]
  26. Inhibition by glucocorticoids of the formation of interleukin-1 alpha, interleukin-1 beta, and interleukin-6: mediation by decreased mRNA stability. Amano, Y., Lee, S.W., Allison, A.C. Mol. Pharmacol. (1993) [Pubmed]
  27. Substance P-induced cyclooxygenase-2 expression in human umbilical vein endothelial cells. Gallicchio, M., Rosa, A.C., Benetti, E., Collino, M., Dianzani, C., Fantozzi, R. Br. J. Pharmacol. (2006) [Pubmed]
  28. Plasmatic vasopressin neurophysin in depression: basic levels and relations with HPA axis. Laruelle, M., Seghers, A., Goffinet, S., Bouchez, S., Legros, J.J. Biol. Psychiatry (1990) [Pubmed]
  29. Decreased steroid responsiveness at night in nocturnal asthma. Is the macrophage responsible? Kraft, M., Hamid, Q., Chrousos, G.P., Martin, R.J., Leung, D.Y. Am. J. Respir. Crit. Care Med. (2001) [Pubmed]
  30. Presence of a transcriptionally active glucocorticoid receptor alpha in lens epithelial cells. James, E.R., Robertson, L., Ehlert, E., Fitzgerald, P., Droin, N., Green, D.R. Invest. Ophthalmol. Vis. Sci. (2003) [Pubmed]
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