Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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Nina Höller

Nariae Baik-Schneditz

Bernhard Schwaberger

Lukas Peter Mileder

Niels Hammer

Gerhard Pichler

Roland Malli

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SHR Neuro Krebs Kardio Lipid Stoffw Microb

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; 31(9):2080-2089 Doi: 10.1161/ATVBAHA.111.231431 [OPEN ACCESS]
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Co-Autor*innen der Med Uni Graz: Heinemann Akos; Konya Viktoria
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Abstract:: Objective-Interleukin (IL)-33 is the most recently described member of the IL-1 family of cytokines and it is a ligand of the ST2 receptor. While the effects of IL-33 on the immune system have been extensively studied, the properties of this cytokine in the cardiovascular system are much less investigated. Methods/Results-We show here that IL-33 promoted the adhesion of human leukocytes to monolayers of human endothelial cells and robustly increased vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and monocyte chemoattractant protein-1 protein production and mRNA expression in human coronary artery and human umbilical vein endothelial cells in vitro as well as in human explanted atherosclerotic plaques ex vivo. ST2-fusion protein, but not IL-1 receptor antagonist, abolished these effects. IL-33 induced translocation of nuclear factor-kappa B p50 and p65 subunits to the nucleus in human coronary artery endothelial cells and human umbilical vein endothelial cells and overexpression of dominant negative form of I kappa B kinase 2 or I kappa B alpha in human umbilical vein endothelial cells abolished IL-33-induced adhesion molecules and monocyte chemoattractant protein-1 mRNA expression. We detected IL-33 and ST2 on both protein and mRNA level in human carotid atherosclerotic plaques. Conclusion-We hypothesize that IL-33 may contribute to early events in endothelial activation characteristic for the development of atherosclerotic lesions in the vessel wall, by promoting adhesion molecules and proinflammatory cytokine expression in the endothelium. (Arterioscler Thromb Vasc Biol. 2011;31:2080-2089.)
Find related publications in this database (using NLM MeSH Indexing): Cell Adhesion -; Cell Adhesion Molecules - biosynthesis; Cells, Cultured -; Endothelial Cells - physiology; Humans -; Inflammation - etiology; Interleukins - physiology; Leukocytes - physiology; NF-kappa B - physiology; Phosphatidylinositol 3-Kinases - physiology; Plaque, Atherosclerotic - etiology; Receptors, Cell Surface - physiology
Find related publications in this database (Keywords): leukocyte adhesion; endothelial cells; IL-33; ST2; atherosclerosis