title: Differential induction of VCAM-1 on human iliac venous and arterial endothelial cells and its role in adhesion.
abstract: Venous and arterial large vessel endothelial cells (EC) were compared for their constitutive and TNF-alpha-induced expression of the cell-surface adhesion molecules ICAM-1 and -2, VCAM-1 and ELAM-1 by FACS analysis. Human iliac venous and arterial EC (HIVEC and HIAEC) constitutively express ICAM-1 and ICAM-2. TNF-alpha increases the expression of ICAM-1, but not ICAM-2, and induces the expression of ELAM-1 on both EC types. However, TNF-alpha induces VCAM-1 cell-surface expression and mRNA only in venous, but not in arterial EC. We next investigated the function of these adhesion molecules and their ligands, LFA-1, very late activation Ag (WLA-L) and sialylated Lewis x glycoprotein (sLe(x)), in adhesion assays with the monocyte-like cell line U937. Untreated U937 cells do not adhere to untreated HIVEC or HIAEC and adhesion is much lower to TNF-alpha-treated arterial than to TNF-alpha-treated venous EC. In adhesion-inhibition assays we demonstrate that U937 cell adhesion to TNF-alpha-treated HIVEC is mediated by VCAM-1/VLA-4 and ELAM-1/sLe(x) interaction, whereas the lower adhesion to TNF-alpha-treated HIAEC is only mediated by ELAM-1/sLe(x) interaction. U937 cells treated with the phorbol ester PMA for 3 days adhere to both HIVEC and HIAEC; this adhesion is mediated by LFA-1 interaction with ICAM-1 and/or -2. Adhesion of PMA-treated U937 cells is increased by TNF-alpha treatment of EC. This increased adhesion is mediated in part by the TNF-alpha-induced VCAM-1 expression on venous EC. Therefore, the cell-surface adhesion molecule VCAM-1 is differentially induced on these two EC types and the differential expression is functionally important in U937 cell adhesion.
authors.affiliation: Department of Pathology, Yale University School of Medicine, New Haven, CT 06510.
authors.forename: I A
authors.initials: IA
authors.lastname: Hauser
authors.forename: D R
authors.initials: DR
authors.lastname: Johnson
authors.forename: J A
authors.initials: JA
authors.lastname: Madri
mesh_terms: D000328:Adult; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000096:biosynthesis* / Q000235:genetics / Q000502:physiology; D002478:Cells, Cultured; D019040:E-Selectin; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D007083:Iliac Artery / Q000378:metabolism*; D007084:Iliac Vein / Q000378:metabolism*; D018799:Intercellular Adhesion Molecule-1; D016169:Lymphocyte Function-Associated Antigen-1 / Q000502:physiology; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis; D016029:Receptors, Very Late Antigen / Q000502:physiology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D015815:Cell Adhesion Molecules; D019040:E-Selectin; D016169:Lymphocyte Function-Associated Antigen-1; D012333:RNA, Messenger; D016029:Receptors, Very Late Antigen; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1; D013755:Tetradecanoylphorbol Acetate