Multifunctional Cytokine Expression by Human Coronary Endothelium and Regulation by Monokines and Glucocorticoids

Effect of high-dose dexamethasone on endothelial haemostatic gene expression and neutrophil adhesion

“…Several studies have shown that cell adhesion molecules, expressed by activated endothelial cells, are responsible for the accumulation of blood leukocytes at sites of inflammation by mediating the adhesion of inflammatory cells to the endothelium [39]. Incubation of endothelial cells with other cytokines such as IL-8 did not significantly alter the expression of the adhesion molecules (ICAM-1, VCAM-1 and E-selectin) [40] although it has been shown that DEXA could effect IL-8 and inhibit its production in different endothelial cell lines [41]. Similarly, DEXA had a small inhibitory effect on constitutive monocyte chemotactic protein-1 (MCP-1) mRNA expression, but no effect on the induction by TNF-␣ [42].…”

Down-modulation of TNFSF15 in ovarian cancer by VEGF and MCP-1 is a pre-requisite for tumor neovascularization

“…It has been reported MCP-1 under certain conditions can be produced by a variety of cell types, including endothelial, fibroblast, epithelial, smooth muscle, mesangial, astrocytic, monocytic, and microglial cells, either constitutively or after induction by oxidative stress, cytokines, or growth factors [18,20,21,50]. MCP-1 has been reported to have an important role in various disease states, including immunodeficiency, cardiovascular, and cancer [51][52][53][54]. Monocytes and macrophages are the major source of MCP-1, however, in many cancers, including ovarian cancer [14][15][16][17].…”

IL-4 stimulates the expression of CXCL-8, E-selectin, VEGF, and inducible nitric oxide synthase mRNA by equine pulmonary artery endothelial cells

“…DXM, a potent glucocorticoid, had been shown to inhibit the CXCL-8 production in response to TNF-␣ by human coronary artery endothelial cells, human pulmonary artery cells, and HUVEC (35). Furthermore, DXM inhibited the upregulation of E-selectin expression in cultured human nasal microvascular endothelial cells stimulated by IL-1␤ and TNF-␣ (65).…”