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Arteriosclerosis, Thrombosis, and Vascular Biology. 1987;7:605-611

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Arteriosclerosis, Vol 7, 605-611, Copyright © 1987 by American Heart Association

ARTICLES

Interleukin-1 inhibits the synthesis of von Willebrand factor in endothelial cells, which results in a decreased reactivity of their matrix toward platelets

PG de Groot, CL Verweij, PP Nawroth, HC de Boer, DM Stern and JJ Sixma
Department of Haematology, University Hospital Utrecht, The Netherlands.

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-1-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.


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