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Titolo:
Dexamethasone inhibits the induction of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase by phorbol ester in human promonocytic U937 cells
Autore:
Tong, M; Tai, HH;
Indirizzi:
Univ Kentucky, Coll Pharm, Div Pharmaceut Sci, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 rmaceut Sci, Lexington, KY 40536 USA
Titolo Testata:
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
fascicolo: 1, volume: 1497, anno: 2000,
pagine: 61 - 68
SICI:
0167-4889(20000602)1497:1<61:DITION>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUCOCORTICOID RECEPTOR; GENE-EXPRESSION; STABLE ANALOGS; PROTEIN-KINASE; HL-60 CELLS; IN-VIVO; SYNTHASE; POTENT; ACID; TRANSACTIVATION;
Keywords:
dexamethasone; prostaglandin; dehydrogenase; inflammation; monocyte;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
36
Recensione:
Indirizzi per estratti:
Indirizzo: Tai, HH Univ Kentucky, Coll Pharm, Div Pharmaceut Sci, Lexington, KY 40536USA Univ Kentucky Lexington KY USA 40536 Sci, Lexington, KY 40536 USA
Citazione:
M. Tong e H.H. Tai, "Dexamethasone inhibits the induction of NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase by phorbol ester in human promonocytic U937 cells", BBA-MOL CEL, 1497(1), 2000, pp. 61-68

Abstract

Pro-inflammatory prostaglandins are known to be first catabolized by NAD(+)-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) to inactive metabolites. This enzyme is under regulatory control by various inflammation-related agents. Regulation of this enzyme was investigated in human promonocytic U937 cells. 15-PGDH activity was found to be optimally induced by phorbol 12-myristate 13-acetate (PMA) at 10 nM after 24 h of treatment. The induction was blocked by staurosporine or CIF 109203X indicating that: the induction was mediated by protein kinase C, The induction by PMA was inhibitedby the concurrent addition of dexamethasone. Nearly complete inhibition was observed at 50 nM, Other glucocorticoids, such as hydrocortisone and corticosterone, but not sex hormones, were also inhibitory. Inhibition by dexamethasone could be reversed by the concurrent addition of antagonist mifepristone (RU-486) indicating that the inhibition was a receptor-mediated event. Either induction by PMA or inhibition by dexamethasone the 15-PGDH activity correlated well with the enzyme protein expression as shown by the Western blot analysis. These results provide the first evidence that prostaglandin catabolism is regulated by glucocorticoids at the therapeutic level. (C)2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 01/04/20 alle ore 11:42:41