PMID: 7544644Sep 1, 1995Paper

Both tumor necrosis factor receptors, TNFR60 and TNFR80, are involved in signaling endothelial tissue factor expression by juxtacrine tumor necrosis factor alpha.

Blood
E F SchmidKlaus Pfizenmaier

Abstract

We have investigated the role of the two distinct tumor necrosis factor (TNF) receptors (TNFR60 and TNFR80) in endothelial cell activation employing an in vitro model of tumor necrosis factor alpha (TNF-alpha)-dependent tissue factor production of human umbilical vein endothelial cells (HUVECs). In this model, tissue factor is produced either on addition of exogeneous TNF-alpha, or by induction of endogenous TNF-alpha via adhesion molecule-linked signal pathways. Under both conditions, tissue factor expression could be partially blocked by antagonistic antibodies against either TNFR60 or TNFR80 and was fully inhibited by simultaneous application of both antibodies. Selective inhibitors of either TNFR60 or TNFR80-induced signal pathways inhibited tissue factor expression, and selective triggering of either of the two TNF receptors by agonistic antibodies induced this response in HUVECs. Furthermore, a coculture system of HUVECs and Chinese hamster ovary transfectants expressing a noncleavable, exclusively membrane-bound form of TNF-alpha resulted in a potent activation of HUVECs with synergistic action of both TNF receptors. Together, these data underline the importance of juxtacrine pathways in endothelial cell activation of pr...Continue Reading

Related Concepts

Related Feeds

Adhesion Molecules in Health and Disease

Cell adhesion molecules are a subset of cell adhesion proteins located on the cell surface involved in binding with other cells or with the extracellular matrix in the process called cell adhesion. In essence, cell adhesion molecules help cells stick to each other and to their surroundings. Cell adhesion is a crucial component in maintaining tissue structure and function. Discover the latest research on adhesion molecule and their role in health and disease here.