My group focuses on the pathogenesis of atherosclerosis with special emphasis on inflammatory activation patterns of cells involved in disease development and progression such as endothelial cells, smooth muscle cells, cardiac myocytes and fibroblasts, monocytes, macrophages, dendritic cells, T-cells and adipocytes. These cells are used in various in vitro models to study processes involved in the development and progression of atherosclerosis, such as inflammatory activation induced by particular cytokines, matrix degradation and remodelling by proteases and angiogenesis and neovascularization. Ongoing projects include investigations on:
- the role of monocyte- and macrophage-subtypes in atherosclerosis
- the involvement of the IL-33/ST2 system in the development and progression of cardiovascular pathologies and obesity and the association between
- the role of inflammatory cells and mediators as a link between obesity and cardiovascular disease
Inflammation and cardiovascular disease
Techniques and infrastructure of the research group
Isolation, characterization and cultivation of human primary cells (endothelial cells and smooth muscle cells from various vascular beds, monocytes, macrophages, preadipocytes, adipocytes, cardiac myocytes and fibroblasts), subtype analysis of human monocytes and macrophages by FACS, adhesion assays to study leukocyte-endothelial interaction under static and flow conditions, access to human tissue (atherosclerotic plaques, heart tissue, adipose tissue), diagnostic and analytical tools (immunohistochemistry, RealTime-PCR, ELISA, Western Blot), Apo E-/- mice as model of atherosclerosis
5 selected publications
Rega G, Kaun C, Weiss TW, Demyanets S, Zorn G, Kastl SP, Steiner S, Seidinger D, Kopp CW, Frey M, Roehle R, Maurer G, Huber K, Wojta J. Inflammatory cytokines interleukin-6 and oncostatin m induce plasminogen activator inhibitor-1 in human adipose tissue. Circulation. 2005 Apr 19;111(15):1938-45.
Hohensinner PJ, Kaun C, Rychli K, Niessner A, Pfaffenberger S, Rega G, Furnkranz A, Uhrin P, Zaujec J, Afonyushkin T, Bochkov VN, Maurer G, Huber K, Wojta J. The inflammatory mediator oncostatin M induces stromal derived factor-1 in human adult cardiac cells. FASEB J. 2009 Mar;23(3):774-82.
Kastl SP, Speidl WS, Katsaros KM, Kaun C, Rega G, Assadian A, Hagmueller GW, Hoeth M, de Martin R, Ma Y, Maurer G, Huber K, Wojta J. Thrombin induces the expression of oncostatin M via AP-1 activation in human macrophages: a link between coagulation and inflammation. Blood. 2009 Sep 24;114(13):2812-8.
Speidl WS, Kastl SP, Hutter R, Katsaros KM, Kaun C, Bauriedel G, Maurer G, Huber K, Badimon JJ, Wojta J. The complement component C5a is present in human coronary lesions in vivo and induces the expression of MMP-1 and MMP-9 in human macrophages in vitro. FASEB J. 2011 Jan;25(1):35-44.
Demyanets S, Konya V, Kastl SP, Kaun C, Rauscher S, Niessner A, Pentz R, Pfaffenberger S, Rychli K, Lemberger CE, de Martin R, Heinemann A, Huk I, Gröger M, Maurer G, Huber K, Wojta J. Interleukin-33 induces expression of adhesion molecules and inflammatory activation in human endothelial cells and in human atherosclerotic plaques. Arterioscler Thromb Vasc Biol. 2011 Sep;31(9):2080-9.