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Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro
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 prod...
Autores principales: | , , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2011
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050730/ https://www.ncbi.nlm.nih.gov/pubmed/21352518 http://dx.doi.org/10.1186/1756-0500-4-40 |
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author | Ruschulte, Heiner Scheinichen, Dirk van Griensven, Martijn Weyrauch, Susanne Liefing, Wibke Harrmeijer, Birgitt Przemeck, Michael Jüttner, Björn |
author_facet | Ruschulte, Heiner Scheinichen, Dirk van Griensven, Martijn Weyrauch, Susanne Liefing, Wibke Harrmeijer, Birgitt Przemeck, Michael Jüttner, Björn |
author_sort | Ruschulte, Heiner |
collection | PubMed |
description | 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. |
format | Text |
id | pubmed-3050730 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30507302011-03-09 Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro Ruschulte, Heiner Scheinichen, Dirk van Griensven, Martijn Weyrauch, Susanne Liefing, Wibke Harrmeijer, Birgitt Przemeck, Michael Jüttner, Björn BMC Res Notes Research Article 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. BioMed Central 2011-02-25 /pmc/articles/PMC3050730/ /pubmed/21352518 http://dx.doi.org/10.1186/1756-0500-4-40 Text en Copyright ©2011 Ruschulte et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Ruschulte, Heiner Scheinichen, Dirk van Griensven, Martijn Weyrauch, Susanne Liefing, Wibke Harrmeijer, Birgitt Przemeck, Michael Jüttner, Björn Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title | Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title_full | Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title_fullStr | Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title_full_unstemmed | Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title_short | Adrenoceptor stimulation does not affect ICAM-1 and VCAM-1 expression in vitro |
title_sort | adrenoceptor stimulation does not affect icam-1 and vcam-1 expression in vitro |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3050730/ https://www.ncbi.nlm.nih.gov/pubmed/21352518 http://dx.doi.org/10.1186/1756-0500-4-40 |
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