MicroRNA-26b Attenuates Platelet Adhesion and Aggregation in Mice.

Peters, Linsey J F; Baaten, Constance C F M J; Maas, Sanne L; Lu, Chang; Nagy, Magdolna; Jooss, Natalie J; Bidzhekov, Kiril; Santovito, Donato; Moreno-Andrés, Daniel; Jankowski, Joachim; Biessen, Erik A L; Döring, Yvonne; Heemskerk, Johan W M; Weber, Christian; Kuijpers, Marijke J E; van der Vorst, Emiel P C (2022). MicroRNA-26b Attenuates Platelet Adhesion and Aggregation in Mice. Biomedicines, 10(5) MDPI 10.3390/biomedicines10050983

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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.

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