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Blood, 15 July 2002, Vol. 100, No. 2, pp. 517-523
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
C5a stimulates production of plasminogen activator inhibitor-1 in
human mast cells and basophils
Johann Wojta,
Christoph Kaun,
Gerlinde Zorn,
Minoo Ghannadan,
Alexander W. Hauswirth,
Wolfgang R. Sperr,
Gerhard Fritsch,
Dieter Printz,
Bernd R. Binder,
Georg Schatzl,
Joerg Zwirner,
Gerald Maurer,
Kurt Huber, and
Peter Valent
From the Departments of Internal Medicine II, Internal
Medicine I, Vascular Biology and Thrombosis Research, and Urology,
University of Vienna, Austria; St Anna Children's Hospital, Vienna,
Austria; and Georg-August University, Goettingen, Germany.
We have recently shown that resting human mast cells (MCs) produce
tissue-type plasminogen activator (t-PA) without simultaneously expressing plasminogen activator inhibitor 1 (PAI-1). In the present study we have identified the anaphylatoxin rhC5a as a potent inducer of
PAI-1 expression in human MCs and basophils. In primary human skin MCs
and primary blood basophils, exposure to rhC5a was followed by an
increase from undetectable to significant levels of PAI-1. In addition,
rhC5a induced a concentration- and time-dependent increase in PAI-1
antigen in the MC line HMC-1 and the basophil cell line KU-812 and
increased the expression of PAI-1 mRNA in HMC-1. In conditioned media
of HMC-1 treated with rhC5a, active PAI-1 could be detected. A
simultaneous loss of t-PA activity in conditioned media from the same
cells indicated that rhC5a-induced PAI-1 was capable of inhibiting the
enzymatic activity of coproduced t-PA. Correspondingly, the levels of
t-PA-PAI-1 complexes increased in rhC5a-treated cells. When HMC-1
cells were incubated with pertussis toxin or anti-C5a receptor
antibodies, the effect of rhC5a on PAI-1 production was completely
abolished. Treatment of C5a with plasmin resulted in loss of its
ability to induce PAI-1 production in MCs. Considering the suggested
role for MCs and components of the complement system in the development
of cardiovascular diseases, we hypothesize that MCs, by producing t-PA
in a resting state and by expressing PAI-1 when activated by C5a, might
participate in the modulation of the balance between proteases and
protease inhibitors regulating tissue injury and repair in such
disease processes.
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