Activation of human endothelial cells by tumor necrosis factor-α results in profound changes in the expression of glycosylation-related genes
✍ Scribed by Juan J. García-Vallejo; Willem Van Dijk; Bert Van Het Hof; Irma Van Die; Marten A. Engelse; Victor W.M. Van Hinsbergh; Sonja I. Gringhuis
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 271 KB
- Volume
- 206
- Category
- Article
- ISSN
- 0021-9541
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
The endothelium plays a central role in the logistics of the immune system by allowing the selective transmigration of leukocytes, as well as the maintenance of the circulation and coagulation homeostasis. Evidence is increasing that the carbohydrate composition of the endothelial cell surface is critical for the cells to exert their physiological function. The major aim of this study is to unravel the mechanisms underlying the expression of carbohydrate structures by endothelial cells, which are involved in leukocyte adhesion and migration. Using quantitative real‐time PCR, the expression profile of a selected group of 74 glycosylation‐related genes has been determined in human umbilical vein endothelial cells (HUVEC) and human foreskin microvascular endothelial cells (FMVEC) under control and TNFα‐induced conditions. The set of genes comprised 59 glycosyltransferases, 6 mannosidases and 9 sulfotransferases. In parallel, the overall cell surface glycan profile has been assessed by the use of glycan‐specific lectins and monoclonal antibodies. The results demonstrate that HUVEC and FMVEC differ substantially in the expression of glycosylation‐related genes and, accordingly, also in the presence of different glycan epitopes on the cell membrane. Induction of an inflamed phenotype of the cells by treatment with TNFα differentially modulates a set of these genes in HUVEC and FMVEC resulting in a change in the cell membrane associated glycans that are of importance in inflammation‐related endothelial cell‐surface processes. © 2005 Wiley‐Liss, Inc.
📜 SIMILAR VOLUMES
Tumor necrosis factor-a (TNF-a) has attracted the greatest attention as a major factor in experimental autoimmune encephalomyelitis (EAE) pathogenesis. We compared rats undergoing EAE with manipulated but healthy animals by examining TNF-a gene expression in cells recovered from the brain. We used r
## BACKGROUND. Previous studies have demonstrated that treatment of human tumor cell lines with a combination of cis-diamminedichloroplatinum (CDDP) and tumor necrosis factor-a (TNF-a) results in additivelsynergistic cytotoxic effects and reverses tumor cell resistance to TNF drugs. Free radical i
## Abstract The proinflammatory cytokine tumor necrosis factor (TNF) α is mainly produced in cells from the monocyte/macrophage lineage. TNFα is also a key signaling molecule in the liver functioning as an important physiological and pathogenic mediator. In hepatocytes or human hepatoma cells TNFα