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-Andres, Daniel; Jankowski, Joachim; Biessen, Erik A. L.; Doering, Yvonne; Heemskerk, Johan W. M.; Weber, Christian; Kuijpers, Marijke J. E. und Vorst, Emiel P. C. van der (2022): MicroRNA-26b Attenuates Platelet Adhesion and Aggregation in Mice. In: Biomedicines, Bd. 10, Nr. 5, 983

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.

• Dokumententyp: Zeitschriftenartikel
• Fakultät: Medizin ; Medizin > Munich Cluster for Systems Neurology (SyNergy)
• Themengebiete: 600 Technik, Medizin, angewandte Wissenschaften > 610 Medizin und Gesundheit
• Sprache: Englisch
• DFG: Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 403584255
• DFG: Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 238187445
• DFG: Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 238187445
• DFG: Gefördert durch die Deutsche Forschungsgemeinschaft (DFG) - 390857198