Funayama H, Sakata Y, Kitagawa S, Ikeda U, Takahashi M, Masuyama J, Mimuro J, Matsuda M, Shimada K
Department of cardiology, Institute of Hematology, Jichi Medical School, Tochigi, Japan.
Thromb Res. 1997 Mar 1;85(5):377-85. doi: 10.1016/s0049-3848(97)00026-1.
Cultured endothelial cells (ECs) produced a constitutive plasminogen activator inhibitor-I (PAI-1), whereas primary culture of monocytes from blood did not produce a detectable amount of PAI-1. Addition of monocytes to ECs caused the accumulation of a large amount of PAI-1 in the supernatant in a dose- and time-dependent manner. Having almost no effect on the production of tissue-type plasminogen activator (t-PA), monocytes decreased the potential fibrinolytic activity of ECs. The 6 hours conditioned medium obtained from the coculture system between monocytes and either ECs or paraformaldehyde-fixed ECs had almost the same effect on the other ECs to produce PAI-1 and t-PA as monocytes that were direct contact with ECs. In addition, this effect was specifically inhibited by using two antibodies against interleukin-1 beta and tumor necrosis factor-alpha. These results indicate that interleukin-1 beta and tumor necrosis factor-alpha induced by the coculture are mostly responsible for decreasing the fibrinolytic activity of ECs.
