Expression of adhesion molecules by cultured human glomerular endothelial cells in response to cytokines: Comparison to human umbilical vein and dermal microvascular endothelial cells

Citation
S. Murakami et al., Expression of adhesion molecules by cultured human glomerular endothelial cells in response to cytokines: Comparison to human umbilical vein and dermal microvascular endothelial cells, MICROVASC R, 62(3), 2001, pp. 383-391
Citations number
28
Categorie Soggetti
Cardiovascular & Hematology Research
Journal title
MICROVASCULAR RESEARCH
ISSN journal
00262862 → ACNP
Volume
62
Issue
3
Year of publication
2001
Pages
383 - 391
Database
ISI
SICI code
0026-2862(200111)62:3<383:EOAMBC>2.0.ZU;2-#
Abstract
We investigated the expression of cell. adhesion molecules on the surface o f glomerular endothelial cells (GEC), dermal microvascular endothelial cell s (MvE), and umbilical vein endothelial cells (HUVEC) that had or had not b een 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 a (TNF-alpha) and interferon-gamma (IFN-gamma). PECA M-1 was a so constitutively expressed on microvascular endothelial cells Mv E 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-d ependent effect on MvE but there was a dose-dependent effect on the level o f expression of cell adhesion molecules on GEC. TNF-alpha induced the expre ssion 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, V CAM-1, and E-selectin different from those seen in HUVEC and MvE upon treat ment with TNF-alpha or IFN-gamma. The use of cultured human GEC allows us t o study not only the inflammatory processes, but also the pathophysiologica l role of GEC in hemodynamic disturbances and their interaction with intrin sic mesangial. cells at the molecular and subcellular levels. (C) 2001 Acad emic Press.