| Autor: |
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 |
| Jazyk: |
angličtina |
| Rok vydání: |
2022 |
| Předmět: |
|
| Zdroj: |
Biomedicines, Vol 10, Iss 5, p 983 (2022) |
| Druh dokumentu: |
article |
| ISSN: |
2227-9059 |
| DOI: |
10.3390/biomedicines10050983 |
| Popis: |
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. |
| Databáze: |
Directory of Open Access Journals |
| Externí odkaz: |
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