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Interleukin‐l Inhibits the Synthesis of von Willebrand Factor in Endothelial Cells, Which Results in a Decreased Reactivity of Their Matrix toward Platelets

Interleukin‐l Inhibits the Synthesis of von Willebrand Factor in Endothelial Cells,... We have studied the influence of recombinant human and murine interleukin-1 (IL-1) on the synthesis and secretion of von Willebrand factor by human endothelial cells. Treatment of endothelial cells with IL-1 caused a decline in the steady-state level of von Willebrand factor mRNA in endothelial cells. This decline resulted in a decreased secretion to the culture medium, a decreased storage of von Willebrand factor in the Weibel-Palade bodies, and a decreased incorporation into the extracellular matrix. As a consequence of the decreased amount of von Willebrand factor in the extracellular matrix we have found a strongly impaired platelet adhesion to these matrices. When the matrices of IL-l-treated cells were incubated with purified von Willebrand factor, their ability to support platelet adhesion was restored. These results suggest that perturbation of endothelial cells by inflammatory mediators like IL-1 results in a decreased adhesion of platelets to the subendothelium owing to a diminished synthesis of von Willebrand factor. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Interleukin‐l Inhibits the Synthesis of von Willebrand Factor in Endothelial Cells, Which Results in a Decreased Reactivity of Their Matrix toward Platelets

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Copyright
© 1987 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

We have studied the influence of recombinant human and murine interleukin-1 (IL-1) on the synthesis and secretion of von Willebrand factor by human endothelial cells. Treatment of endothelial cells with IL-1 caused a decline in the steady-state level of von Willebrand factor mRNA in endothelial cells. This decline resulted in a decreased secretion to the culture medium, a decreased storage of von Willebrand factor in the Weibel-Palade bodies, and a decreased incorporation into the extracellular matrix. As a consequence of the decreased amount of von Willebrand factor in the extracellular matrix we have found a strongly impaired platelet adhesion to these matrices. When the matrices of IL-l-treated cells were incubated with purified von Willebrand factor, their ability to support platelet adhesion was restored. These results suggest that perturbation of endothelial cells by inflammatory mediators like IL-1 results in a decreased adhesion of platelets to the subendothelium owing to a diminished synthesis of von Willebrand factor.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Nov 1, 1987

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