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Arteriosclerosis, Thrombosis, and Vascular Biology. 1990;10:129-134

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Arteriosclerosis, Vol 10, 129-134, Copyright © 1990 by American Heart Association

ARTICLES

Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion

F Breviario, P Proserpio, F Bertocchi, MG Lampugnani, A Mantovani and E Dejana
Istituto di Ricerche Farmacologiche Mario Negri, Milan, Italy.

Interleukin-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGI2). This was accompanied by endogenous 3H-arachidonic acid (3H-AA) release and by a time-dependent increase in the cells' ability to convert exogenous AA. The continuous presence of IL-1 was not required, but about a 1-hour stimulation with the cytokine was sufficient to trigger the cells to synthesize PGI2 for several hours. The spectrum of 3H-AA conversion shows that, in addition to 6-keto-prostaglandin F1 alpha, prostaglandin F2 alpha also was raised after IL-1. The recovery of PGI2 synthesis after aspirin was faster in IL-1-treated EC than in control cells. These data define some of the characteristics of IL-1 stimulation of PGI2 and suggest that this process is mediated both by endogenous AA mobilization and by an increase in cyclooxygenase activity.


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