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Lysoplasmenylcholine increases neutrophil adherence to human coronary artery endothelial cells.
- Source :
-
American journal of physiology. Cell physiology [Am J Physiol Cell Physiol] 2007 Nov; Vol. 293 (5), pp. C1467-71. Date of Electronic Publication: 2007 Aug 29. - Publication Year :
- 2007
-
Abstract
- We demonstrated previously that thrombin stimulation of human coronary artery endothelial cells (HCAEC) results in release of choline lysophospholipids [lysophosphatidylcholine (lysoPtdCho) and lysoplasmenylcholine (lysoPlsCho)]. These amphiphilic metabolites have been implicated in arrhythmogenesis following the onset of myocardial ischemia, but studies examining their direct effects on the vasculature remain limited. We and others have shown that thrombin and lysoPtdCho can increase cell surface adhesion molecules and adherence of circulating inflammatory cells to the endothelium. This study supports our hypothesis that these changes may be mediated, at least in part, by lysoPlsCho, thus implicating this metabolite as an inflammatory mediator in the coronary vasculature and a modulator of the progression of atherosclerosis. Apical stimulation of HCAEC with thrombin resulted in the production and release of choline lysophospholipids from the apical surface of the HCAEC monolayer. Basolateral stimulation had no effect on choline lysophospholipid production or release from either the apical or basolateral surface of the HCAEC monolayer. Incubation of HCAEC with lysoPlsCho or lysoPtdCho resulted in similar increases in HCAEC surface expression of P-selectin and E-selectin. Furthermore, lysoPlsCho increased cell surface expression of P-selectin, E-selectin, vascular cell adhesion molecule-1, and intercellular adhesion molecule-1 with a time course similar to that of thrombin stimulation. Increased presence of cell surface adhesion molecules may contribute to the significant increase in adherence of neutrophils to either thrombin- or lysoPlsCho-stimulated HCAEC. These results demonstrate that the presence of thrombin at sites of vascular injury in the coronary circulation, resulting in increased choline lysophospholipid release from the HCAEC apical surface, has the potential to propagate vascular inflammation by upregulation of adhesion molecules and recruitment of circulating inflammatory cells to the endothelium.
- Subjects :
- Cells, Cultured
Coronary Artery Disease metabolism
Coronary Vessels cytology
E-Selectin metabolism
Humans
Intercellular Adhesion Molecule-1 metabolism
Lysophosphatidylcholines metabolism
P-Selectin metabolism
Time Factors
Vascular Cell Adhesion Molecule-1 metabolism
Cell Adhesion
Coronary Vessels metabolism
Endothelial Cells metabolism
Inflammation Mediators metabolism
Lysophospholipids metabolism
Neutrophils metabolism
Thrombin metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 0363-6143
- Volume :
- 293
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- American journal of physiology. Cell physiology
- Publication Type :
- Academic Journal
- Accession number :
- 17728394
- Full Text :
- https://doi.org/10.1152/ajpcell.00290.2007