session

61 - Oral Communication
Mechanisms of Disease I
Feb. 25, 2021, 1:45 p.m. - 3:15 p.m., Rome

Abstract

5
WITHDRAWN - Impact of platelets and red blood cells in abdominal aortic aneurysm
K. J. Krott, M. Wagenhäuser, A. Ehrenberg, T. Feige, A. Beele, E. Schickentanz-Dey, H. Schelzig, M. Elvers, Presenter: K. J. Krott (Düsseldorf)

Background and Objective
Abdominal aortic aneurysm (AAA) represents a vascular disease with high morbidity and mortality. Recent clinical trials revealed no benefit administering potential growth restrictors; thus, no therapeutic approach is available to date. Certain factors have been shown to increase the risk for an AAA, e.g. smoking, high blood pressure and vascular inflammation. 80% of all AAAs are accompanied by a growing platelet-rich intraluminal thrombus (ILT) that might be relevant for AAA progression. The interaction of platelets (plts) and red blood cells (RBCs) is important for thrombus formation in hemostasis and thrombosis. However, the impact of platelets and RBCs in AAA progression and the consequences for ILT formation are poorly understood.
Methods
Flow cytometry analysis was performed with whole blood from AAA patients and mice using the angiotensin II and the PPE mouse model. Histological sections of the ILT and the aortic wall were stained with specific markers for RBCs, platelets and thrombospondin-1 (TSP-1). Plasma levels of TSP-1 and CD36 were determined in AAA patients.
Results
First, platelet activation was measured by the analysis of active platelet integrin αIIbβ3 and the surface exposure of P-selectin as marker for degranulation using resting and activated platelets form AAA patients and experimental mice. In addition, increased PS exposure at the membrane of platelets and RBCs from AAA patients revealed enhanced pro-coagulant activity of these cells compared to age-matched healthy volunteers. As a first marker of platelet and RBC interactions in AAA, flow cytometric analysis of whole blood samples from AAA patients detected increased binding of TSP-1 to the platelet surface and elevated externalization of CD36 on the RBC surface. Histological sections of the ILT and the aortic wall were stained with specific markers for platelets, RBCs and TSP-1 and showed an accumulation of TSP-1 and platelet-RBC aggregates. Furthermore, the plasma levels of TSP-1 and CD36 were increased in AAA patients compared to age-matched healthy volunteers.
Conclusion
Taken together, platelets showed a pre-activated state in AAA disease. Enhanced PS and CD36 on RBCs of AAA patients and accumulation of TSP-1 and platelet-RBC aggregates in the ILT suggest that these mechanisms might play a prominent role in AAA progression.
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