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 language | English |
---|---|
Article number | 983 |
Number of pages | 14 |
Journal | Biomedicines |
Volume | 10 |
Issue number | 5 |
DOIs | |
Publication status | Published - May 2022 |
Keywords
- EXPRESSION
- FAMILY
- GLYCOPROTEIN-VI
- GROWTH
- KIDNEY
- KINASES
- PACKAGE
- PATHWAY
- RECEPTOR
- SURVIVAL
- cardiovascular diseases
- microRNA-26b
- microRNAs
- platelets
- thrombosis