MicroRNA-26b Attenuates Platelet Adhesion and Aggregation in Mice

Linsey J F Peters, Constance C F M J Baaten, Sanne L Maas, Chang Lu, Magdolna Nagy, Natalie J Jooss, Kiril Bidzhekov, Donato Santovito, Daniel Moreno-Andrés, Joachim Jankowski, Erik A L Biessen, Yvonne Döring, Johan W M Heemskerk, Christian Weber, Marijke J E Kuijpers, Emiel P C van der Vorst*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Platelets are key regulators of haemostasis, making platelet dysfunction a major driver of thrombosis. Numerous processes that determine platelet function are influenced by microRNAs (miRs). MiR-26b is one of the highest-expressed miRs in healthy platelets, and its expression in platelets is changed in a diseased state. However, the exact effect of this miR on platelet function has not been studied yet. In this study, we made use of a whole-body knockout of miR-26b in ApoE-deficient mice in order to determine its impact on platelet function, thrombus formation and platelet signalling both ex vivo and in vivo. We show that a whole-body deficiency of miR-26b exacerbated platelet adhesion and aggregation ex vivo. Additionally, in vivo, platelets adhered faster, and larger thrombi were formed in mice lacking miR-26b. Moreover, isolated platelets from miR-26b-deficient mice showed a hyperactivated Src and EGFR signalling. Taken together, we show here for the first time that miR-26b attenuates platelet adhesion and aggregation, possibly through Src and EGFR signalling.

Original languageEnglish
Article number983
Number of pages14
JournalBiomedicines
Volume10
Issue number5
DOIs
Publication statusPublished - May 2022

Keywords

  • EXPRESSION
  • FAMILY
  • GLYCOPROTEIN-VI
  • GROWTH
  • KIDNEY
  • KINASES
  • PACKAGE
  • PATHWAY
  • RECEPTOR
  • SURVIVAL
  • cardiovascular diseases
  • microRNA-26b
  • microRNAs
  • platelets
  • thrombosis

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