Abstract
The effect of interleukin-1 (IL-1) and tumor necrosis factor (TNF) on the fibrinolytic system of vascular wall was investigated using cultured endothelial cell (EC) . The fibrinolytic potential may depend on the net balance of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAT) . Both IL-1 and TNF stimulated the PAT production of EC in a dose dependent manner without changing the production of t-PA.
TNF was demonstrated to induce IL-1 production by EC. Since the effect of TNF was not inhibited by neutralization with antibodies to IL-1α and IL-1β, the effect of TNF on PAI production may not have been mediated by the endogenous generation of IL-1.
As we previously reported that IL-1 and TNF additively induced PGI2 synthesis of EC, the effect of PGI2 on API production of EC was evaluated. Both PGI2 and forskolin, an activation of adenylate cyclase, decreased PAI production of EC PGI2 may compensate the induction of PAT production of EC by IL-1 and TNF.
These data might indicate that cytokines could play an important role on the regulation of fibrinolytic system of vascular endothelial cells.
