Publications by authors named "Marianna Gyenes"

Article Synopsis
  • Shear stress activates platelet signaling that can lead to increased blood clotting, playing a role in heart attacks; the study focuses on how a specific genetic variation (Leu33Pro polymorphism) in a platelet integrin affects this process.
  • Researchers exposed platelets with different genotypes to normal and high shear stress, measuring key signaling markers (Src and FAK) related to platelet activation.
  • The findings reveal that high shear stress significantly enhances Src and FAK activity in both genotypes, but Pro33 platelets showed higher activity overall, indicating that this genetic variation influences how platelets respond to shear stress.
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Platelet integrin αIIbβ3 possesses a Leu/Pro polymorphism at residue 33 (Leu33/HPA-1a or Pro33/HPA-1b). The Pro33 isoform has been suggested to exhibit prothrombotic features. αIIbβ3-expressing CHO (Chinese hamster ovary) cells on immobilized fibrinogen show activation of the MAP kinase family member ERK2, with an enhanced ERK2 activity in Pro33 cells compared to Leu33 cells.

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: Shear stress alone can activate platelets resulting in a subsequent platelet aggregation, so-called 'shear-induced platelet aggregation'. In our work, we analyzed how differently elevated shear stress impacts the Src and focal adhesion kinase (FAK) activation in fibrinogen-adherent human platelets. We detected the extents of Src pY418 and FAK pY397 activations in platelets on immobilized fibrinogen and over BSA under shear conditions.

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Fibronectin (FN), a dimeric adhesive glycoprotein, which is present both in plasma and the extracellular matrix can interact with platelets and thus contribute to platelet adhesion and aggregation. It has been shown that FN can decrease platelet aggregation but enhance platelet adhesion, suggesting a dual role of FN in haemostasis. The prevalent function(s) of FN may be determined by its fibril form.

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