Key result
Oral intake of 500mg aspirin reduced the magnitude of platelet Ca2+ responses and lowered the intra-individual coefficients of variance of the responses by 50%.
Why the study?
Does oral aspirin reduce the inter-individual variability of Ca2+ signaling in platelets from healthy volunteers?
Observational (n=51)
Does oral aspirin reduce the inter-individual variability of Ca2+ signaling in platelets from healthy volunteers?
Inter-individual variability in platelet Ca2+ signaling persists despite aspirin intake and is partly determined by the expression levels of specific SERCA isoforms.
Aspirin may reduce intra-individual platelet Ca2+ variability in healthy volunteers; leaves open whether persistent inter-individual differences affect clinical outcomes.
Increased Ca2+ signal generation may lead to hyperactivity of platelets and contribute to thrombotic complications. Using fura-2-loaded platelets from 51 healthy volunteers, high variability was detected in the Ca2+ responses evoked by the receptor agonists, thrombin and collagen, and the inhibitor of sarco/endoplasmic reticulum Ca2+-ATPases (SERCA), thapsigargin (Tg). Oral intake of 500mg aspirin reduced the magnitude of the Ca2+ responses, and lowered the intra-individual coefficients of variance of the responses by 50%. However, the corresponding inter-individual variance coefficients were only a little influenced by aspirin intake, pointing to subject-dependent factors in Ca2+ handling that are unrelated to thromboxane formation. With each agonist, 6-9% of the subjects had platelets with relatively high Ca2+ responses (> mean + SD) both before and after aspirin intake. In 90% (9/10) of these cases the high responsiveness was confirmed in platelets obtained 6-12 months later. The Tg- but not thrombin-induced Ca2+ responses correlated inversely with the expression levels of SERCA PL/IM 430 (SERCA-3b) in platelets. After aspirin intake, the Ca2+ responses with collagen but not thrombin correlated inversely with SERCA-2b expression. These results suggest that, in the absence of potentiating effects of thromboxane, (i) the amount of PL/IM 430-recognizable SERCA may control the Ca2+ signal when SERCA-2b is specifically inhibited (with Tg), and (ii) the expression of SERCA-2b determine the collagen- but not the thrombin-evoked Ca2+ signal. Accordingly, limited Ca2+-pumping activity by low expression of one of the SERCA isoforms is likely to be one of the factors resulting in increased platelet activity towards collagen or thapsigargin but not thrombin.
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Feijge et al. (1998) conducted an observational in Healthy volunteers (n=51). Aspirin vs. Baseline (before aspirin intake) was evaluated on Ca2+ responses evoked by thrombin, collagen, and thapsigargin. Oral intake of 500mg aspirin reduced the magnitude of platelet Ca2+ responses and lowered the intra-individual coefficients of variance of the responses by 50%.
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