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Aspirin treatment hampers the use of plasma microRNA-126 as a biomarker for the progression of vascular disease

Hetty C. de Boer, Coen van Solingen, Jurriën Prins, Jacques M.G.J. Duijs, Menno V. Huisman, Ton J. Rabelink, Anton Jan van Zonneveld
DOI: http://dx.doi.org/10.1093/eurheartj/eht007 First published online: 5 February 2013

Abstract

Aims MicroRNA-126 (miR-126) facilitates angiogenesis and regulates endothelial cell function. Recent data suggest that miR-126 can serve as a biomarker for vascular disease. Although endothelial cells are enriched for miR-126, platelets also contain miR-126. In this paper, we investigated the contribution of platelets to the pool of miR-126 in plasma of patients with type 2 diabetes (DM2) and how this is affected by aspirin.

Methods and 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, monitored in patients with DM2 by measuring soluble P-selectin, correlated directly with circulating levels of miR-126. The administration of aspirin resulted both in platelet inhibition and concomitantly reduced circulating levels of platelet-derived microRNAs including miR-126.

Conclusion Platelets are a major source of circulating miR-126. Consequently, in patho-physiological conditions associated with platelet activation, such as diabetes type 2, the administration of aspirin may lead to reduced levels of circulating miR-126. Thus, the use of platelet inhibitors should be taken into account when using plasma levels of miR-126 as a biomarker.

  • miR-126
  • platelets
  • aspirin
  • diabetes mellitus type 2
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