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Volume 272, Number 49, Issue of December 5, 1997 pp. 31065-31072
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.

Tumor Necrosis Factor- Inversely Regulates Prostaglandin D₂ and Prostaglandin E₂ Production in Murine Macrophages
SYNERGISTIC ACTION OF CYCLIC AMP ON CYCLOOXYGENASE-2 EXPRESSION AND PROSTAGLANDIN E₂ SYNTHESIS

(Received for publication, August 21, 1997, and in revised form, September 22, 1997)

From the Division of Basic Sciences, Department of Pediatrics, National Jewish Center for Immunology and Respiratory Medicine, Denver, Colorado 80206

Increased synthesis of insulin-like growth factor-1 is induced in murine macrophages by prostaglandin E₂ (PGE₂) and tumor necrosis factor- (TNF). Accordingly, we have investigated mechanisms regulating synthesis of PGE₂ that might contribute to autocrine/paracrine effects on insulin-like growth factor-1 production. In response to zymosan, TNF specifically induced a 5-fold increase in PGE₂ synthesis, at the same time decreasing PGD₂ production in a reciprocal fashion. Activators of cyclic AMP-dependent protein kinase (PKA), such as PGE₂ itself or dibutyryl cyclic AMP, did not modify PGE₂ production by themselves but potentiated the TNF-induced increase in PGE₂; this effect required both RNA and protein synthesis. No significant change in arachidonate release or production of other eicosanoids was observed. The inducible form of cyclooxygenase-2 (COX2) but not of the constitutive form COX1 was implicated in the generation of both PGE₂ and PGD₂ in these cells by use of specific inhibitors and effects of dexamethasone. Neither COX1 nor COX2 protein levels were affected by TNF or PKA activators used alone, whereas in association, marked up-regulation of COX2 mRNA and protein was observed. Incubations of cells carried out with PGH₂ demonstrated that PGE₂ synthase activity was increased after a TNF pretreatment. Taken together, our results suggest that TNF induced a switch from the PGD₂ to PGE₂ synthesis pathway by regulating PGE₂ synthase expression and/or activity and that activators of PKA markedly potentiated the TNF-induced increase in PGE₂ through up-regulation of COX2 gene expression.

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