Gamma-interferon induces prostacyclin and prostaglandin but not lipoxygenase product synthesis in rat endothelial cells

Immunology Letters
P Mattila, R Renkonen

Abstract

The major arachidonic acid metabolites excreted by untreated rat heart endothelial cells were prostacyclin (PGI2), 5-hydroxyeicosatetraenoic acid (5-HETE) and 15-hydroxyeicosatetraenoic acid (15-HETE). Trace amounts of both prostaglandin E (PGE) and thromboxane B2 (TXB2) were also produced. The activity of leukotriene B4 (LTB4) was the same as baseline activity. Gamma-interferon (gamma-IFN) treatment increased the production of PGI2 and PGE more than three-fold compared to control values. Thromboxane production increased two-fold while the excretion of 5-HETE and 15-HETE was unaffected. No LTB4 excretion was seen after gamma-IFN stimulus. Methylprednisolone downregulated the 5-HETE, 15-HETE and prostacyclin production both in normal and gamma-IFN treated cells. Indomethacin decreased prostacyclin excretion in untreated cells and also decreased gamma-IFN-induced prostacyclin and PGE excretion. Taken together these results indicate that rat microvascular endothelial cells excrete prostaglandins and prostacyclin, but not leukotrienes.

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Citations

Mar 1, 1995·Journal of Clinical Pharmacology·A F BenslimaneL Welin
Oct 1, 1993·Prostaglandins, Leukotrienes, and Essential Fatty Acids·S Hyslop, G De Nucci
Sep 1, 1993·Prostaglandins, Leukotrienes, and Essential Fatty Acids·K WatanabeM Yoshida
Oct 1, 1992·Prostaglandins, Leukotrienes, and Essential Fatty Acids·A Ristimäki, L Viinikka
Jul 1, 1996·European Journal of Immunology·K M StuhlmeierF H Bach
May 1, 1992·Prostaglandins, Leukotrienes, and Essential Fatty Acids·A PinsonE Shohami

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