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Hemodynamic forces modulate the effects of cytokines on fibrinolytic
activity of endothelial cells
Y Kawai, Y Matsumoto, K Watanabe, H Yamamoto, K Satoh, M Murata, M Handa and Y Ikeda
Departments of Laboratory Medicine, Keio University School of Medicine,
Tokyo, Japan.
We investigated the effects of hemodynamic force on fibrinolytic activity
of cultured human umbilical vein endothelial cells stimulated by cytokines,
using a modified cone-plate viscometer in which well- controlled and
-defined shear forces were generated. Treatment of the cells with
interleukin (IL)-beta or tumor necrosis factor alpha (TNFalpha) under
static conditions had no effect on tissue plasminogen activator (t-PA)
secretion, while release of plasminogen activator inhibitor 1 (PAI-1)
increased. When cells were exposed to increasing shear stress up to 24
dynes/cm2, levels of t-PA and t-PA/PAI-1 complex significantly increased
relative to shear stress, while total PAI-1 and active PAI-1 secretion
decreased gradually. In the presence of IL-1beta or TNFalpha, the increase
in production of t-PA and the t-PA/PAI-1 complex was further augmented. Dot
blot hybridization analysis of cultured cells in similar experimental
conditions using t-PA and PAI-1 cDNA probes revealed no t-PA mRNA in 3
microg total RNA from static endothelial cells under resting or
cytokine-stimulated conditions, but abundant t-PA mRNA was detected in
cells subjected to a shear force of 18 dynes/cm2, and the increase was
further augmented by addition of cytokines. In contrast, PAI-1 mRNA was
detected in resting and cytokine- stimulated, nonsheared endothelial cells,
but levels decreased after exposure to shear stress, even in the presence
of cytokines. These results indicate a role for hemodynamic forces in
regulating fibrinolytic activity with or without cytokine stimulation.
Volume 87,
Issue 6,
pp. 2314-2321,
03/15/1996
Copyright © 1996 by The American Society of Hematology
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