Does Platelet FcγRIIA Really Amplify Thrombosis on Its Own? – RPTH Journal
RPTH Journal shared a post on LinkedIn about a recent article by Florian Tupin et al, adding:
“Does platelet FcγRIIA really amplify thrombosis on its own?
FcγRIIA plays a well established role in immune mediated platelet activation and immunothrombosis. But whether it also enhances conventional platelet activation and arterial thrombosis without an FcγRIIA specific trigger has remained controversial.
In this new Хэштег RPTH study, Tupin and colleagues revisited this question using human platelets alongside transgenic mice expressing human FcγRIIA.
Blocking FcγRIIA did not alter human platelet aggregation to ADP, collagen, CRP, TRAP, or U46619. FcγRIIA expressing and WT mice showed comparable:
- Platelet aggregation and thrombus formation under flow
- Tail bleeding
- FeCl₃ induced carotid thrombosis
- Mechanical injury induced aortic thrombosis
- Laser-induced mesenteric arterial thrombosis
Together, the findings challenge the proposed role of FcγRIIA as an amplifier of αIIbβ3 outside in signaling and suggest an important distinction: FcγRIIA may be critical when FcγRIIA specific extracellular stimuli are present, but appears dispensable for hemostasis and experimental arterial thrombosis in their absence.”
Title: Platelet FcγRIIA is dispensable for hemostasis and arterial thrombosis in the absence of FcγRIIA specific extracellular stimuli
Authors: Florian Tupin, Stephanie Magnenat, Clarisse Mouriaux, Pierre H. Mangin, Béatrice Hechler
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