Atherosclerosis; Cardiovascular Diseases; Inflammation; Thrombosis
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
Techniques, methods & infrastructure
Techniques, methods 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
- Cellular mediators linking inflammation and thrombosis | leader of the project part "Coagulatory Phenotypes of Monocyte and Macrophage Subsets" (2013)
Source of Funding: FWF (Austrian Science Fund), Special Research Programmes (SFB54)
- MicroRNA expression profiling of patients with Carotid Artery Stenosis undergoing Endarterectomy: the miRNA CASE – Study (2013)
Source of Funding: OeNB (Oesterreichische Nationalbank), Anniversary Fund
- Inflammation and Obesity, leader of the project part "Angiogenesis and Inflammation in Adipose Tissue: A link between obesity and cardiovascular disease (0)
Source of Funding: LBG (Ludwig Boltzmann Gesellschaft), LB Cluster for Cardiovascular Research
- Hohensinner, P.J. et al., 2020. Alternative activation of human macrophages enhances tissue factor expression and production of extracellular vesicles. Haematologica, p.haematol.2019.220210. Available at: http://dx.doi.org/10.3324/haematol.2019.220210.
- Thaler, B. et al., 2019. Differential expression of Plg-RKT and its effects on migration of proinflammatory monocyte and macrophage subsets. Blood, 134(6), pp.561–567. Available at: http://dx.doi.org/10.1182/blood.2018850420.
- Hohensinner, P.J. et al., 2017. PAI-1 (Plasminogen Activator Inhibitor-1) Expression Renders Alternatively Activated Human Macrophages Proteolytically Quiescent. Arteriosclerosis, Thrombosis, and Vascular Biology, 37(10), pp.1913–1922. Available at: http://dx.doi.org/10.1161/ATVBAHA.117.309383.
- Speidl, W.S. et al., 2010. 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. The FASEB Journal, 25(1), pp.35-44. Available at: http://dx.doi.org/10.1096/fj.10-156083.
- Kastl, S.P. et al., 2009. Thrombin induces the expression of oncostatin M via AP-1 activation in human macrophages: a link between coagulation and inflammation. Blood, 114(13), pp.2812-2818. Available at: http://dx.doi.org/10.1182/blood-2009-01-200915.