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Chemical Compound Review

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

Synonyms:
 
 
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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

References

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  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]
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  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]
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