My laboratory studies inflammatory mechanisms involved in the development of atherosclerosis. Oxidized lipoproteins profoundly change the function of macrophages in atherosclerotic lesions. We study the role of 12/15-lipoxygenase and Toll-like receptors in the macrophage inflammatory responses. The hypothesis being tested is that 12/15LO-mediated modification of LDL produces ligands that activate TLR4 and other cellular receptors. Thus, we study macrophage signaling pathways and gene expression, macropinocytosis and phagocytosis of apoptotic cells as characteristics of macrophage activation in vascular inflammation.
A new exciting direction in our research is studying the processes of vascular inflammation in zebrafish. The optical transparency of zebrafish larvae enables monitoring vascular lipid and macrophage accumulation in real time in a live animal. This opens endless possibilities for in vivo functional studies of certain processes of atherogenesis.