Reyhan Nergiz-Unal

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BACKGROUND Atherothrombosis is a major cause of cardiovascular events. However, animal models to study this process are scarce. OBJECTIVES We describe the first murine model of acute thrombus formation upon plaque rupture to study atherothrombosis by intravital fluorescence microscopy. METHODS Localized rupture of an atherosclerotic plaque in a carotid(More)
The glycoprotein CD36, also known as glycoprotein IIIb/IV or FAT, is expressed on the surface of platelets, monocytes, microvascular endothelial cell, smooth muscle cells, cardiomyocytes and other cells of the cardiovascular system. In spite of its abundant presence, CD36 has remained for long a mysterious protein with a poorly understood role. In this(More)
OBJECTIVE Platelets abundantly express the membrane receptor CD36 and store its ligand thrombospondin-1 (TSP1) in the α-granules. We investigated whether released TSP1 can support platelet adhesion and thrombus formation via interaction with CD36. APPROACH AND RESULTS Mouse platelets deficient in CD36 showed reduced adhesion to TSP1 and subsequent(More)
The fibrin(ogen) receptor, integrin αIIbβ3, has a well-established role in platelet spreading, aggregation and clot retraction. How αIIbβ3 contributes to platelet-dependent coagulation is less well resolved. Here, we demonstrate that the potent suppressing effect of clinically used αIIbβ3 blockers on tissue factor-induced thrombin generation is linked to(More)
BACKGROUND In most models of experimental thrombosis, healthy blood vessels are damaged. This results in the formation of a platelet thrombus that is stabilized by ADP signaling via P2Y(12) receptors. However, such models do not predict involvement of P2Y(12) in the clinically relevant situation of thrombosis upon rupture of atherosclerotic plaques. We(More)
BACKGROUND AND OBJECTIVE Platelets abundantly express glycoprotein CD36 with thrombospondin-1 (TSP1) and oxidized low-density lipoprotein (oxLDL) as proposed ligands. How these agents promote platelet activation is still poorly understood. METHODS AND RESULTS Both TSP1 and oxLDL caused limited activation of platelets in suspension. However, immobilized(More)
Activation of AMP-activated protein kinase (AMPK) in cardiomyocytes induces translocation of glucose transporter GLUT4 and long-chain fatty acid (LCFA) transporter CD36 from endosomal stores to the sarcolemma to enhance glucose and LCFA uptake, respectively. Ca(2+)/calmodulin-activated kinase kinase-β (CaMKKβ) has been positioned directly upstream of AMPK.(More)
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