Dexamethasone inhibits mitogen induction of the TIS10 prostaglandin synthase/cyclooxygenase gene

J Biol Chem. 1992 Apr 25;267(12):7991-4.

Abstract

Glucocorticoids block the induced secretion of prostaglandins in a variety of biological contexts. We have identified a primary response gene, TIS10, which encodes a mitogen-inducible prostaglandin synthase/cyclooxygenase in Swiss 3T3 cells. TIS10 is distinct from prostaglandin synthase/cyclooxygenase. (EC 1.14.99.1), previously cloned from mouse, man, and sheep. Dexamethasone blocks prostaglandin E2 synthesis by 3T3 cells in response to tetradecanoylphorbol acetate. Dexamethasone also blocks both phorbol ester- and forskolin-induced TIS10 mRNA accumulation. In contrast, phorbol esters, forskolin, and dexamethasone have little or no effect on the levels of prostaglandin synthase/cyclooxygenase mRNA in 3T3 cells. Moreover, dexamethasone does not inhibit induction of TIS8/egr-1, another primary response gene. Inhibition of the synthesis of TIS10 prostaglandin synthase/cyclooxygenase may be a principal mechanism by which glucocorticoids block prostaglandin synthesis and secretion.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • 3T3 Cells
  • Animals
  • Blotting, Northern
  • Colforsin / pharmacology
  • Dexamethasone / pharmacology*
  • Dinoprostone / biosynthesis
  • Mice
  • Mitogens*
  • Prostaglandin-Endoperoxide Synthases / genetics*
  • RNA, Messenger / biosynthesis
  • RNA, Messenger / drug effects
  • Radioimmunoassay
  • Tetradecanoylphorbol Acetate / pharmacology

Substances

  • Mitogens
  • RNA, Messenger
  • Colforsin
  • Dexamethasone
  • Prostaglandin-Endoperoxide Synthases
  • Dinoprostone
  • Tetradecanoylphorbol Acetate