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Ruschulte H, Scheinichen D, van Griensven M, et al. Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro. BMC Res Notes. 2011;4:40doi: 10.1186/1756-0500-4-40.
Ruschulte, H., Scheinichen, D., van Griensven, M., Weyrauch, S., Liefing, W., Harrmeijer, B., Przemeck, M., & Jüttner, B. (2011). Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro. BMC research notes, 440. https://doi.org/10.1186/1756-0500-4-40
Ruschulte, Heiner, et al. "Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro." BMC research notes vol. 4 (2011): 40. doi: https://doi.org/10.1186/1756-0500-4-40
Ruschulte H, Scheinichen D, van Griensven M, Weyrauch S, Liefing W, Harrmeijer B, Przemeck M, Jüttner B. Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro. BMC Res Notes. 2011 Feb 25;4:40. doi: 10.1186/1756-0500-4-40. PMID: 21352518; PMCID: PMC3050730.
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BMC Res Notes. 2011 Feb 25;4:40. doi: 10.1186/1756-0500-4-40.

Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro.

BMC research notes

Heiner Ruschulte, Dirk Scheinichen, Martijn van Griensven, Susanne Weyrauch, Wibke Liefing, Birgitt Harrmeijer, Michael Przemeck, Björn Jüttner

Affiliations

  1. Dept, of Anaesthesiology & Intensive Care Medicine, Hannover Medical School Hannover, Germany. [email protected].

PMID: 21352518 PMCID: PMC3050730 DOI: 10.1186/1756-0500-4-40

Abstract

BACKGROUND: Endothelial adhesion molecules ICAM-1 (CD54) and VCAM-1 (CD106) mediate cellular adhesion and transcellular migration. Cell adhesion and diapedesis have a key role in the course of shock and sepsis. During severe sepsis, adrenoceptor agonist levels may be increased due to endogenous production or due to intensive care treatment. As yet, the influence of β1 or β2 agonists on adhesion molecule formation on endothelial cells has remained unclear.

METHODS: Cultured human umbilical vein endothelial cells were stimulated with E. coli. Following bacterial stimulation the cells were incubated with either β2 receptor agonist terbutaline or β1 agonist norepinephrine. ICAM-1 and VCAM-1 expression were examined using flow cytometry.

RESULTS: Administration of norepinephrine did not cause increases of both CD54 and CD106 in stimulated HUVEC. Compared to negative controls the bacterial stimulation itself led to an increase of adhesion molecules. Following administration of terbutaline no significant increase in CD54 expression was found.

CONCLUSIONS: Bacterial stimulation led to an increase of adhesion molecule expression. Adrenoceptor stimulation of activated endothelial cells did not cause significant increases of cellular adhesion molecules.

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