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Cyclosporine a inhibits tissue factor expression in monocytes/macrophages
H Holschermann, F Durfeld, U Maus, A Bierhaus, K Heidinger, J Lohmeyer, PP Nawroth, H Tillmanns and W Haberbosch
Department of Internal Medicine, Justus-Liebig-University Giessen, Germany.
Accelerated coronary atherosclerosis in cardiac allografts is the major
limiting factor for long-term survival after heart transplantation. There
is growing evidence that activation of the coagulation mechanism is
involved in the development of transplant atherosclerosis. Tissue factor
(TF) expression by cells of the monocyte/macrophage system may represent an
important mechanism underlying the fibrin deposition in the affected
vessels. In the present study, we investigated the effect of cyclosporine A
(CsA) on the lipopolysaccharide (LPS)-induced procoagulant activity (PCA)
in human monocytes/macrophages. CsA exerted a dose-dependent inhibitory
effect on LPS-induced monocyte/macrophage PCA, which was identified as TF
activity based on functional and immunologic characterization. As shown by
reverse transcriptase- polymerase chain reaction, CsA reduced the
transcription of the TF gene in LPS-stimulated monocytes/macrophages.
Electrophoretic mobility shift assay showed that CsA inhibited the
LPS-induced activation of the nuclear factor kappa B (NF-kappa B). As shown
by Western blot analysis, CsA treatment decreased the nuclear translocation
of NF-kappa B, thereby suggesting the mechanism for the inhibitory effect
of CsA on TF induction. Hence, a nonimmunologic effect of CsA may
contribute to its successful use in transplant medicine.
Volume 88,
Issue 10,
pp. 3837-3845,
11/15/1996
Copyright © 1996 by The American Society of Hematology
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