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Platelet-derived growth factor release and antiplatelet treatment with low-dose acetylsalicylic acid
H Vissinger1, S E Husted, S D Kristensen
1University Department of Medicine and Cardiology, Aarhus County Hospital, Denmark.
Insights
Low-dose aspirin (ASA) significantly inhibits the release of platelet-derived growth factor (PDGF) and beta-thromboglobulin (beta-TG) from platelets when stimulated by collagen. This finding suggests a potential mechanism for aspirin
Area of Science:
- Cardiovascular Medicine
- Pharmacology
- Hematology
Background:
- Platelet-derived growth factor (PDGF) and beta-thromboglobulin (beta-TG) are released during platelet activation.
- PDGF is implicated in atherosclerosis and restenosis post-percutaneous transluminal coronary angioplasty (PTCA).
- Acetylsalicylic acid (ASA) is a common antiplatelet medication.
Purpose of the Study:
- To investigate the effect of low-dose acetylsalicylic acid (ASA) on PDGF and beta-TG release.
- To assess ASA's impact on thromboxane B2 (TxB2) synthesis.
- To understand ASA's role in collagen-induced platelet activation.
Main Methods:
- Healthy volunteers ingested 300 mg of ASA.
- Measurements of PDGF, beta-TG, and TxB2 were performed using radioimmunoassay (RIA).
- Analyses were conducted in serum and platelet-rich plasma (PRP) before and after ASA ingestion, with submaximal collagen stimulation.
Main Results:
- In serum, ASA significantly reduced TxB2 levels but did not affect PDGF or beta-TG.
- In PRP, ASA significantly decreased collagen-induced PDGF, beta-TG, and TxB2 release.
- TxB2 synthesis in both PRP and serum was significantly inhibited by ASA.
Conclusions:
- Low-dose ASA effectively inhibits collagen-induced release of beta-TG and PDGF in platelet-rich plasma.
- ASA significantly reduces TxB2 synthesis in both PRP and serum.
- These findings highlight a potential mechanism for ASA's therapeutic effects in cardiovascular conditions involving platelet activation.
Abstract:
Platelet-derived growth factor (PDGF) and beta-thromboglobulin (beta-TG) are released from alpha granules during platelet activation. PDGF may play a role in the development of atherosclerosis and the late restenosis after percutaneous transluminal coronary angioplasty (PTCA). The effect of acetylsalicylic acid (ASA) on PDGF release was studied in healthy volunteers before and twelve hours after ingestion of 300 mg ASA. PDGF, beta-TG, and thromboxane B2(TxB2) were measured by radioimmunoassay (RIA) in serum and in platelet rich plasma (PRP) after submaximal stimulation with collagen. TxB2 decreased significantly from 0.9 +/- 0.3 ng/(mL x 10(6) platelets) to 0.006 +/- 0.005 ng/(mL x 10(6) platelets) (mean +/- SD) in serum after ASA ingestion while PDGF and beta-TG remained unchanged. Measurements in PRP after stimulation with collagen showed a significant decrease in PDGF (from 21.5 +/- 1.4 pg/(mL x 10(6) platelets) to 1.8 +/- 4.1 (pg/mL x 10(6) platelets), in beta-TG (from 21.0 +/- 13.3 ng/(mL x 10(6) platelets) to 2.2 +/- 1.4 ng/(mL x 10(6) platelets)) and in TxB2 (from 143.6 +/- 80.7 pg/(mL x 10(6) platelets) to 0.5 +/- 0.6 pg/(mL x 10(6) platelets)) after treatment with ASA. In conclusion low-dose ASA inhibits collagen-induced release of both beta-TG and PDGF in PRP and TxB2-synthesis in PRP and serum.