Contribution of ICAM-1 and VCAM-1 to the morphological changes in monocytes bound to human venous endothelial cells stimulated with recombinant interleukin-4 (rIL-4) or rIL-1 alpha.
The present study focused on the question of whether the expression of intracellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on the surface of cultured human venous endothelial cells (EC), stimulated with recombinant interleukin-4 (rIL-4) or rIL-1 alpha, contributes to the stretching of human monocytes following their binding to EC. Stimulation of monolayers of venous EC with rIL-4 for 24 hr induced marked expression of VCAM-1 but not ICAM-1 on EC, increased the adhesiveness of EC for monocytes but did not promote stretching of EC-bound monocytes over the surface of EC. Stimulation of EC with rIL-1 alpha for 24 hr induced surface expression of both ICAM-1 and VCAM-1, enhanced the binding of monocytes to EC and increased the percentage of EC-bound monocytes with a stretched morphology about 2.7-fold. Anti-ICAM-1 but not anti-VCAM-1 mAb markedly reduced the percentage stretched monocytes on rIL-1 alpha-stimulated EC. We conclude that ICAM-1 but not VCAM-1 on cytokine-stimulated EC is essential for the stretching of EC-bound monocytes.
D002448:Cell Adhesion / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000502:physiology*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D007375:Interleukin-1 / Q000502:physiology; D015847:Interleukin-4 / Q000502:physiology; D007378:Interleukins / Q000502:physiology*; D009000:Monocytes / Q000166:cytology* / Q000378:metabolism; D011994:Recombinant Proteins; D019010:Vascular Cell Adhesion Molecule-1
D015815:Cell Adhesion Molecules; D007375:Interleukin-1; D007378:Interleukins; D011994:Recombinant Proteins; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D015847:Interleukin-4