title: Expression of adhesion molecules by cultured human glomerular endothelial cells in response to cytokines: comparison to human umbilical vein and dermal microvascular endothelial cells.
abstract: We investigated the expression of cell adhesion molecules on the surface of glomerular endothelial cells (GEC), dermal microvascular endothelial cells (MvE), and umbilical vein endothelial cells (HUVEC) that had or had not been stimulated by cytokines. PECAM-1 was constitutively expressed at a high level on HUVEC but its expression level decreased following stimulation by tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma). PECAM-1 was also constitutively expressed on microvascular endothelial cells MvE and GEC, but at lower levels than on HUVEC, and expression by these cells also decreased in response to TNF-alpha and IFN-gamma. There was no dose-dependent effect on MvE but there was a dose-dependent effect on the level of expression of cell adhesion molecules on GEC. TNF-alpha induced the expression of VCAM-1 on HUVEC and GEC, but not MvE, while IFN-gamma induced VCAM-1 expression only on HUVEC. TNF-alpha induced the expression of E-selectin on all three kinds of endothelial cells, but IFN-gamma had no effect on E-selectin expression. GEC therefore showed expression patterns of PECAM-1, VCAM-1, and E-selectin different from those seen in HUVEC and MvE upon treatment with TNF-alpha or IFN-gamma. The use of cultured human GEC allows us to study not only the inflammatory processes, but also the pathophysiological role of GEC in hemodynamic disturbances and their interaction with intrinsic mesangial cells at the molecular and subcellular levels.
authors.affiliation: Department of Cellular Physiology, Institute of Nephrology, Niigata University Faculty of Medicine, Niigata 951-8510, Japan.
authors.forename: S
authors.initials: S
authors.lastname: Murakami
authors.forename: T
authors.initials: T
authors.lastname: Morioka
authors.forename: Y
authors.initials: Y
authors.lastname: Nakagawa
authors.forename: Y
authors.initials: Y
authors.lastname: Suzuki
authors.forename: M
authors.initials: M
authors.lastname: Arakawa
authors.forename: T
authors.initials: T
authors.lastname: Oite
mesh_terms: D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002470:Cell Survival; D002478:Cells, Cultured; D016207:Cytokines / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D019040:E-Selectin / Q000096:biosynthesis / Q000187:drug effects / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D006801:Humans; D007365:Intercellular Junctions / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology; D007678:Kidney Glomerulus / Q000098:blood supply*; D008562:Membrane Glycoproteins / Q000378:metabolism; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000187:drug effects / Q000378:metabolism*; D012867:Skin / Q000098:blood supply; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D014471:Umbilical Veins / Q000166:cytology; D019010:Vascular Cell Adhesion Molecule-1 / Q000187:drug effects / Q000378:metabolism*
chemical_list: D015815:Cell Adhesion Molecules; D016207:Cytokines; D019040:E-Selectin; D008562:Membrane Glycoproteins; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D014409:Tumor Necrosis Factor-alpha; D019010:Vascular Cell Adhesion Molecule-1; D007371:Interferon-gamma