Blood Journal
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Platelets activated during myocardial infarction release functional miRNA, which can be taken up by endothelial cells and regulate ICAM1 expression

  1. Olof Gidlöf1,
  2. Marcel van der Brug2,
  3. Jenny Öhman1,
  4. Patrik Gilje1,
  5. Björn Olde1,
  6. Claes Wahlestedt2, and
  7. David Erlinge1
  1. 1Department of Cardiology, Faculty of Medicine, Lund University, Lund, Sweden; and
  2. 2Department of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, Miami, FL

Key Points

  • Patients with myocardial infarction have altered platelet miRNA profiles.

  • Activated platelets release miRNAs that can be taken up by endothelial cells and regulate ICAM-1 gene expression.


Platelets play a crucial role in the pathogenesis of myocardial infarction (MI) by adhering to the site of a ruptured atherosclerotic plaque. The aim of this study was to screen for differences in the micro RNA (miRNA) content of platelets from patients with myocardial infarction and control patients, to investigate a possible release of miRNAs from activated platelets and to elucidate whether platelet-derived miRNAs could act as paracrine regulators of endothelial cell gene expression. Using RNA-seq, we found 9 differentially expressed miRNAs in patients compared with healthy controls, of which 8 were decreased in patients. Of these, miR-22, -185, -320b, and -423-5p increased in the supernatant of platelets after aggregation and were depleted in thrombi aspirated from MI patients, indicating the release of certain miRNAs from activated platelets. To confirm that endothelial cells could take up the released platelet miRNAs, transfer of both fluorescently labeled miRNA and exogenous cel-miR-39 from activated platelets to endothelial cells was shown. Finally, a possible paracrine role of released platelet miR-320b on endothelial cell intercellular adhesion molecule-1 expression was shown. Thus, platelets from patients with MI exhibit loss of specific miRNAs, and activated platelets shed miRNAs that can regulate endothelial cell gene expression.

  • Submitted October 15, 2012.
  • Accepted March 8, 2013.
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