As thrombotic events are responsible for the lethal consequences of atherosclerosis, the central importance of blood platelets to this disease has been recognized for many years. Nevertheless, current literature provides compelling evidence that platelets and their activation state are not only involved in the final stages of atherosclerosis but rather play a key role in the development of this – as well as other - diseases, as stimulated platelets are causally involved in the onset of inflammatory reactions, cell proliferation and immune responses.

In turn, the platelet proteome and platelet activation pathways are affected by (inflammation-derived) oxidative stress and several types of metabolic or age-related diseases.

Our group studies a wide range of platelet-related aspects, including platelet-leukocyte interaction and the direct interaction of distinct pathogens with platelets.

Currently we focus on the following topics: platelet function:

• pro-inflammatory and immune-modulatory effects of oxidatively modified lipoproteins on platelet function
• anti-inflammatory effects of high density lipoproteins
• immune-modulatory role of (activated) platelets and their interaction with leukocytes
• influence of smoking and sedentary lifestyle on platelet reactivity and microparticle formation

Research topic

Oxidative stress and platelet function –platelets as modulators of inflammation

Techniques and infrastructure of the research group

Flow cytometer with two laser lines (480nm / 640nm) for quantification of platelet-leukocyte aggregates, expression of platelet-specific antigens and activation-dependent surface markers as well as quantification of intracellular phosphoproteins relevant to platelet function. Platelet-specific functional tests (aggregometry, platelet adhesion). Advanced molecular and cellular biology techniques, cell culture, transgenic mouse models.

5 selected publications

   1.   Badrnya S, Butler LM, Soderberg-Naucler C, Volf I and Assinger A. Platelets directly enhance neutrophil transmigration in response to oxidised low-density lipoprotein. Thromb Haemost 108: 719-729, 2012.

   2.   Hoetzenecker K, Assinger A, Lichtenauer M, Mildner M, Schweiger T, Starlinger P, Jakab A, Berenyi E, Pavo N, Zimmermann M, Gabriel C, Plass C, Gyongyosi M, Volf I and Ankersmit HJ. Secretome of apoptotic peripheral blood cells (APOSEC) attenuates microvascular obstruction in a porcine closed chest reperfused acute myocardial infarction model: role of platelet aggregation and vasodilation. Basic Res Cardiol 107: 292, 2012.

   3.   Assinger A, Laky M, Schabbauer G, Hirschl A, Buchberger E, Binder BR and Volf I. Efficient phagocytosis of periodontopathogens by neutrophils requires plasma factors, platelets and TLR2. J Thromb Haemost 9: 799-809, 2011.

   4.   Assinger A, Koller F, Schmid W, Zellner M, Babeluk R, Koller E and Volf I. Specific binding of hypochlorite-oxidized HDL to platelet CD36 triggers proinflammatory and procoagulant effects. Atherosclerosis 212: 153-160, 2010.

   5.   Assinger A, Koller F, Schmid W, Zellner M, Koller E and Volf I. Hypochlorite-oxidized LDL induces intraplatelet ROS formation and surface exposure of CD40L--a prominent role of CD36. Atherosclerosis 213: 129-134, 2010.