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 α (TNF-α) and interferon γ (IFN-γ). 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-α and IFN-γ. 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-α induced the expression of VCAM-1 on HUVEC and GEC, but not MvE, while IFN-γ induced VCAM-1 expression only on HUVEC. TNF-α induced the expression of E-selectin on all three kinds of endothelial cells, but IFN-γ 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-α or IFN-γ. 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.

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