Interleukin-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGl2). 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 PGl2 for several hours. The spectrum of 3H-AA conversion shows that, in addition to 6-ketoprostaglandin F1α, prostaglandin F2αalso was raised after IL-1. The recovery of PGl2 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 PGl2 and suggest that this process is mediated both by endogenous AA mobilization and by an increase in cyclooxygenase activity.
|Number of pages||6|
|Journal||Arteriosclerosis, Thrombosis, and Vascular Biology|
|Publication status||Published - 1990|
- Endothelial cells
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine