Mast cells are thought to play an important role in atherogenesis and plaqu
e rupture, but their role in the subsequent platelet activation and thrombu
s formation is unclear. Tryptase positive cells (KU812(T+)) were establishe
d from the KU812 cell line as an in vitro model of human mast cells and use
d to study the effect of mast cell activation on human platelets, Overnight
incubation of KU812(T+) with IgE and subsequent challenge with anti-IgE ca
used the release of heparinoid substances which inhibited 1 mu g/ml collage
n-induced platelet aggregation. KU812(T+) challenged with compound 48/80 pr
oduced a releasate that had no apparent heparinoid content but caused full
platelet aggregation. These findings showed that, although activation of KU
812(T+) via Fc epsilon R1 partially abrogated collagen-induced platelet agg
regation, activation of the C5a receptor signalling pathway, by compound 48
/80, caused the release of potent platelet-activating substances. This cell
culture model offers a unique insight into the role of platelet-mast cell
interactions in arterial thrombogenesis.