Figure 4
Figure 4. Aspirin decreases agonist-induced release of platelet cytokines. Equal volumes of platelets (2.5 × 108) were stimulated with ADP, TRAP, and collagen in the presence and absence of low-dose aspirin (20 μM) and the releasate was incubated with human cytokine protein antibody arrays (A). The intensity of each cytokine on the array in the presence (■) and absence (□) of low-dose aspirin with each agonist is compared (B). Signals for platelet-derived growth factor (PDGF) (i), growth regulating growth factor (GRO) (ii), angiogenin (Ang) (iii), and oncostatin M (OSM) (iv) are shown (mean ± SD of 3 independent experiments with different donors). Signal intensities for different donors were normalized to the positive control spots (C).

Aspirin decreases agonist-induced release of platelet cytokines. Equal volumes of platelets (2.5 × 108) were stimulated with ADP, TRAP, and collagen in the presence and absence of low-dose aspirin (20 μM) and the releasate was incubated with human cytokine protein antibody arrays (A). The intensity of each cytokine on the array in the presence (■) and absence (□) of low-dose aspirin with each agonist is compared (B). Signals for platelet-derived growth factor (PDGF) (i), growth regulating growth factor (GRO) (ii), angiogenin (Ang) (iii), and oncostatin M (OSM) (iv) are shown (mean ± SD of 3 independent experiments with different donors). Signal intensities for different donors were normalized to the positive control spots (C).

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