2.50
Hdl Handle:
http://hdl.handle.net/10755/161438
Type:
Presentation
Title:
Upregulation of a Cell Adhesion Molecule by 5-Hydroxytryptamine
Abstract:
Upregulation of a Cell Adhesion Molecule by 5-Hydroxytryptamine
Conference Sponsor:Midwest Nursing Research Society
Conference Year:2003
Author:Gordon, Joanne
Contact Address:Biomedical Sciences, 901 S. National Avenue, Springfield, MO, 65804, USA
The purpose of this study was to determine whether 5-hydroxytryptamine (5-HT, serotonin) can upregulate vascular cell adhesion molecules (VCAM) on cultured human umbilical vein endothelial cells (HUVECs). During inflammation, leukocytes leave the vascular bed and travel to the site of tissue injury. Endothelial cells are integrally involved by providing a surface for leukocyte attachment. The mechanisms for leukocyte adhesion and extravasation involve a number of inflammatory cytokines and a variety of adhesion molecules and their ligands. Tumor necrosis factor-alpha (TNF), an inflammatory cytokine released by activated macrophages, increases the number of adhesion molecules typically found on endothelial cells, including selectins and other adhesion molecules (ICAM, VCAM, and PECAM). Initially, neutrophils bind loosely to selectins, then tumble down the endothelial cell, ultimately binding tightly to ICAM and VCAM. This binding facilitates further attachment of the neutrophil to PECAM, located at intercellular junctions, leading to migration of the neutrophil to the subendothelial space by diapedesis. Although the literature supports TNF upregulation of VCAM, little is known about the role of 5-HT in the upregulation of this adhesion molecule. Released from aggregating platelets, 5-HT is present during inflammation, causing increased vascular permeability and smooth muscle contraction in local arterioles and venules. In this study, one group of cells were exposed to TNF, known to upregulate VCAM; another group was exposed to 5-HT; a third group served as the control. At the end of 12 hour exposure to the cytokines, VCAM was detected using immunofluorescent techniques. The findings confirm that TNF can upregulate VCAM. This study also provides evidence for 5-HT upregulation of VCAM on HUVECs, thus suggesting an additional mechanism that facilitates movement of leukocytes to the site of inflammation. Ongoing research is exploring factors that influence upregulation of VCAM by 5-HT. AN: MN030367
Repository Posting Date:
26-Oct-2011
Date of Publication:
17-Oct-2011
Sponsors:
Midwest Nursing Research Society

Full metadata record

DC FieldValue Language
dc.typePresentationen_GB
dc.titleUpregulation of a Cell Adhesion Molecule by 5-Hydroxytryptamineen_GB
dc.identifier.urihttp://hdl.handle.net/10755/161438-
dc.description.abstract<table><tr><td colspan="2" class="item-title">Upregulation of a Cell Adhesion Molecule by 5-Hydroxytryptamine </td></tr><tr class="item-sponsor"><td class="label">Conference Sponsor:</td><td class="value">Midwest Nursing Research Society</td></tr><tr class="item-year"><td class="label">Conference Year:</td><td class="value">2003</td></tr><tr class="item-author"><td class="label">Author:</td><td class="value">Gordon, Joanne</td></tr><tr class="item-address"><td class="label">Contact Address:</td><td class="value">Biomedical Sciences, 901 S. National Avenue, Springfield, MO, 65804, USA</td></tr><tr><td colspan="2" class="item-abstract">The purpose of this study was to determine whether 5-hydroxytryptamine (5-HT, serotonin) can upregulate vascular cell adhesion molecules (VCAM) on cultured human umbilical vein endothelial cells (HUVECs). During inflammation, leukocytes leave the vascular bed and travel to the site of tissue injury. Endothelial cells are integrally involved by providing a surface for leukocyte attachment. The mechanisms for leukocyte adhesion and extravasation involve a number of inflammatory cytokines and a variety of adhesion molecules and their ligands. Tumor necrosis factor-alpha (TNF), an inflammatory cytokine released by activated macrophages, increases the number of adhesion molecules typically found on endothelial cells, including selectins and other adhesion molecules (ICAM, VCAM, and PECAM). Initially, neutrophils bind loosely to selectins, then tumble down the endothelial cell, ultimately binding tightly to ICAM and VCAM. This binding facilitates further attachment of the neutrophil to PECAM, located at intercellular junctions, leading to migration of the neutrophil to the subendothelial space by diapedesis. Although the literature supports TNF upregulation of VCAM, little is known about the role of 5-HT in the upregulation of this adhesion molecule. Released from aggregating platelets, 5-HT is present during inflammation, causing increased vascular permeability and smooth muscle contraction in local arterioles and venules. In this study, one group of cells were exposed to TNF, known to upregulate VCAM; another group was exposed to 5-HT; a third group served as the control. At the end of 12 hour exposure to the cytokines, VCAM was detected using immunofluorescent techniques. The findings confirm that TNF can upregulate VCAM. This study also provides evidence for 5-HT upregulation of VCAM on HUVECs, thus suggesting an additional mechanism that facilitates movement of leukocytes to the site of inflammation. Ongoing research is exploring factors that influence upregulation of VCAM by 5-HT. AN: MN030367 </td></tr></table>en_GB
dc.date.available2011-10-26T23:21:21Z-
dc.date.issued2011-10-17en_GB
dc.date.accessioned2011-10-26T23:21:21Z-
dc.description.sponsorshipMidwest Nursing Research Societyen_GB
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