title: Mechanism of ATP-induced leukocyte adherence to cultured pulmonary artery endothelial cells.
abstract: Previously we have shown that ATP enhances the adherence of HL-60 cells and human neutrophils to bovine pulmonary artery endothelial cells. The current investigations extend earlier findings by showing that ATP and UTP dose-dependently stimulate human neutrophil adherence to human pulmonary artery endothelial cells. We have also explore the mechanisms of ATP- and UTP-stimulated adherence. We have found that fucose, a component of selectin receptors, inhibits ATP-stimulated HL-60 cell-bovine pulmonary artery endothelial cell adhesion. Additionally, pretreatment of HL-60 cells with neuraminidase abolishes ATP enhancement. However, fucose does not affect ATP- or thrombin-induced adhesion of freshly isolated human neutrophils to human endothelial cells. Antibodies to human P-selection intercellular adhesion molecule (ICAM)-1, and the beta-subunit of CD11/CD18 do not alter ATP-induced adherence of HL-60 cells to bovine endothelial cells. Similarly, antibodies to human P-selectin and ICAM-1 do not inhibit human neutrophil-human pulmonary artery endothelial cell adhesion. The platelet-activating factor receptor antagonists, WEB-2086 and L-659,989, are effective in attenuating ATP- and UTP-stimulated adherence. Preincubation of neutrophils or human pulmonary artery endothelial cells with ATP or UTP also enhances adherence, an effect that is blocked by L-659,989. Thus platelet activating factor, associated with both neutrophils and endothelial cells, mediates ATP- and UTP-induced neutrophil adherence. ATP, released during vascular injury, may exacerbate neutrophil-endothelial cell interaction and thereby contribute to neutrophil-induced injury.
authors.affiliation: Department of Medicine, Providence Veterans Affairs Medical Center, Rhode Island, USA.
authors.forename: A L
authors.initials: AL
authors.lastname: Parker
authors.forename: L L
authors.initials: LL
authors.lastname: Likar
authors.forename: D D
authors.initials: DD
authors.lastname: Dawicki
authors.forename: S
authors.initials: S
authors.lastname: Rounds
mesh_terms: D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D000906:Antibodies / Q000276:immunology; D002417:Cattle; D002448:Cell Adhesion; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000502:physiology*; D005643:Fucose / Q000494:pharmacology; D018922:HL-60 Cells / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007962:Leukocytes / Q000187:drug effects* / Q000502:physiology; D008358:Mannose / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000502:physiology; D010969:Plastics; D010980:Platelet Membrane Glycoproteins / Q000037:antagonists & inhibitors; D011651:Pulmonary Artery / Q000166:cytology / Q000502:physiology*; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; D014544:Uridine Triphosphate / Q000494:pharmacology
chemical_list: D000906:Antibodies; D010969:Plastics; D010980:Platelet Membrane Glycoproteins; D011956:Receptors, Cell Surface; D043562:Receptors, G-Protein-Coupled; C039351:platelet activating factor receptor; D005643:Fucose; D000255:Adenosine Triphosphate; D008358:Mannose; D014544:Uridine Triphosphate