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Journal of Endotoxin Research
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Lipopolysaccharide-induced proliferation and adhesion of U937 cells to endothelial cells involves barium chloride sensitive hyperpolarization

Ali Erdogan

Department of Cardiology and Angiology, Justus-Liebig-University of Giessen, Giessen, Germany, Ali.Erdogan{at}med.uni-giessen.de

Christian Alexander Schaefer

Department of Cardiology and Angiology, Justus-Liebig-University of Giessen, Giessen, Germany

Astrid Kerstin Most

Department of Cardiology and Angiology, Justus-Liebig-University of Giessen, Giessen, Germany

Martina Barbara Schaefer

Department of Pulmonology, Justus-Liebig-University of Giessen, Giessen, Germany

Konstantin Mayer

Department of Pulmonology, Justus-Liebig-University of Giessen, Giessen, Germany

Harald Tillmanns

Department of Cardiology and Angiology, Justus-Liebig-University of Giessen, Giessen, Germany

Christoph Ruediger Wolfram Kuhlmann

Department of Cardiology and Angiology, Justus-Liebig-University of Giessen, Giessen, Germany

The adhesion of monocytes to the endothelium and their proliferation in the subendothelial space play an important role in atherosclerosis. Since the proliferation and migration of cells are influenced by the activity of ion channels, the aim of this study was to examine whether barium chloride (Ba2+)-sensitive potassium channels (KiCa) are involved in lipopolysaccharide (LPS)-induced proliferation of monocytic U937 cells, and in the adhesion of these cells to endothelial cells. The adhesion of LPS-stimulated U937 cells to endothelial cells reached a maximum at a concentration of 5 µg/ml. This effect of LPS was completely abolished in the presence of Ba2+ (100 µmol/l). In addition, LPS-induced proliferation was significantly reduced by Ba 2+ (control, 100%; LPS 5 µg/ml, 175%; LPS + Ba2+ 100 µmol/l, 136%; n = 12, P < 0.05). To examine whether KiCa are activated by LPS, changes of U937 membrane potential were determined. LPS (5 µg/ml) caused a hyperpolarization of U937 cells indicating a flux of K+ ions out of the cells. This effect was completely blocked by Ba2+ (100 µmol/l). In conclusion, we demonstrate that LPS activates KiCa in U937 cells, which is responsible for LPS-induced adhesion of these cells to endothelial cells, and to the proliferation of U937 cells.

Key Words: U937 • endothelial cells • adhesion • proliferation • lipopolysaccharide • potassium channels

Journal of Endotoxin Research, Vol. 12, No. 4, 224-230 (2006)
DOI: 10.1177/09680519060120040301
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