Abstract 487: Aspirin Treatment Hampers the Use of Plasma MicroRNA-126 as Biomarker for the Progression of Vascular Disease
Rationale MicroRNA-126 (miR-126) facilitates angiogenesis and regulates endothelial cell function. Recent data suggest that miR-126 can serve as a biomarker for cardiovascular disease. Although endothelial cells are enriched for miR-126, platelets also comprise a major pool of miR-126. We investigated the contribution of platelets to the level of miR-126 circulating in the plasma from patients with type 2 diabetes and how this level is affected by aspirin.
Methods & Results In vitro platelet activation resulted in the transfer of miR-126 from the platelet- to the plasma-compartment, which was prevented by aspirin. In vivo platelet activation was studied in patients with type 2 diabetes, who exhibit disease-mediated platelet activation and are prone to develop cardiovascular disease. Platelet activation was monitored by measuring soluble P-selectin in plasma and correlated significantly with circulating levels of miR-126. Administration of aspirin to the patients in a randomized, placebo-controlled cross-over design, resulted in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including miR-126.
Conclusion The profile of circulating miRs constitutes a fingerprint of activated platelets rather then activated endothelial cells. In particular miR-126 can be derived from activated platelets and the circulating levels of this miRNA can be markedly reduced when aspirin is used in patho-physiological conditions associated with platelet activation such as diabetes type 2. Therefore, the use of platelet inhibitors should be taken into account when using plasma-levels of miR-126 as a biomarker.
- © 2013 by American Heart Association, Inc.