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Interleukin‐1 Stimulates Prostacyclin Production by Cultured Human Endothelial Cells by Increasing Arachidonic Acid Mobilization and Conversion

Interleukin‐1 Stimulates Prostacyclin Production by Cultured Human Endothelial Cells by... Interieukln-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGI2). This was accompanied by endogenous3H-arachldonlc acid f H-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 cytoklne was sufficient to trigger the cells to synthesize PGI2for several hours. The spectrum of3H-AA conversion shows that, In addition to 6-ketoprostaglandln F1α, prostaglandln F2α, also was raised after IL-1. The recovery of PGI2synthesis 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 PGI2and suggest that this process Is mediated both by endogenous AA mobilization and by an increase In cyclooxygenase activity. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Interleukin‐1 Stimulates Prostacyclin Production by Cultured Human Endothelial Cells by Increasing Arachidonic Acid Mobilization and Conversion

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Copyright
© 1990 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Interieukln-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGI2). This was accompanied by endogenous3H-arachldonlc acid f H-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 cytoklne was sufficient to trigger the cells to synthesize PGI2for several hours. The spectrum of3H-AA conversion shows that, In addition to 6-ketoprostaglandln F1α, prostaglandln F2α, also was raised after IL-1. The recovery of PGI2synthesis 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 PGI2and suggest that this process Is mediated both by endogenous AA mobilization and by an increase In cyclooxygenase activity.

Journal

Arteriosclerosis – Wolters Kluwer Health

Published: Jan 1, 1990

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