Synergy of Recombinant Tumor Necrosis Factor and Endotoxins against Meth A Tumors in vivo and Endothelial Cells in vitro1

2015 ◽  
pp. 171-176 ◽  
Author(s):  
Nanne Bloksma ◽  
Paul A. van de Wiel ◽  
C. Frieke Kuper ◽  
Frans M. A. Hofhuis
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

Effects of recombinant tumor necrosis factor (rHuTNFα)on human neutrophils and monocytes: In vitro, ex vivo and in vivo

2009 ◽  
Vol 43 (4) ◽  
pp. 286-296 ◽  
Author(s):  
E. Schell-Frederick ◽  
T. Tepass ◽  
G. Lorscheidt ◽  
M. Pfreundschuh ◽  
M. Schaadt ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Ex Vivo ◽  
Human Neutrophils ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

Growth Inhibition of Human Endothelial Cells by Human Recombinant Tumor Necrosis Factor Alpha and Interferon-Gamma

1994 ◽  
Vol 80 (4) ◽  
pp. 301-305 ◽  
Author(s):  
Thekla Mauerhoff ◽  
Antonino Belfiore ◽  
Ricardo Pujol-Borrell ◽  
Gian Franco Bottazzo
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Proliferative Response ◽  
Tumor Necrosis ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Ifn Γ ◽  
Recombinant Tumor Necrosis Factor ◽  
Necrosis Factor

We investigated the effect of recombinant tumor necrosis factor-alpha (rTNF- α) on the proliferative response of human umbilical vein endothelial cells (HUVEC) to normal human serum (NHS), in the absence or the presence of interferon (IFN)- γ. rTNF- α significantly impaired NHS-stimulated HUVEC growth at a dose as low as 0.1 U/ml. The inhibitory effect of rTNF- α was dose-dependent up to 50-100 U/ml and was already evident after 2 h of incubation. Doses of rTNF- α in the range of 10 U/ml completely suppressed 3H-thymidine uptake stimulated by 7.5% NHS, and the effect was partially overcome by 10-20% NHS. rTNF- α was not cytotoxic at doses up to 1000 U/ml. rIFN- γ was also effective in suppressing NHS-stimulated3H-thymidine incorporation, and at low doses (0.1 U/ml) rIFN- γ and rTFN- α showed an additive effect. The effect of TFN- α and IFN- γ in antagonizing the proliferative response of vascular endothelium to the variety of growth factors contained in human serum could be relevant in a variety of pathologic conditions involving endothelium damage and proliferation.

TUMOR NECROSIS FACTOR INCREASES THE PRODUCTION OF PLASMINOGEN ACTIVATOR INHIBITOR IN HUMAN ENDOTHELIAL CELLS IN VITRO AND IN RATS IN VIVO

1987 ◽  
Author(s):  
V W M van Hinsbergh ◽  
T Kooistra ◽  
W Fiers ◽  
J J Emeis
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Activator Inhibitor ◽  
Necrosis Factor ◽  
Stimulation Of

The vascular endothelium plays an important role in fibrinolysis by producing tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI). The production of these factors by cultured endothelial cells (EC) is under separate control and influenced by various mediators, such as interleukin-1 (IL-1). Similar to IL-1, the monokine tumor necrosis factor (TNF) induces in EC various membrane bound components: tissue factor, HLA-A,B antigens and leukocyte adhesion molecules. We here report that TNF increased the production of PAI by human EC and increased PAI plasma levels in rats.In the presence of serum, TNF increased the production of PAI by cultured human EC from umbilical vein (2-fold) and from foreskin microvessels (2 to 10-fold). This was demonstrated by titration of t-PA to a fixed amount of EC conditioned medium, by reverse fibrin autography, and by immunoprecipitation with specific anti-PAI-1 IgG. No change in t-PA activity was found by fibrin autography. The stimulation of PAI activity by TNF was found at 4 U/ml and reached a maximum at 500 U/ml; it was not prevented by the addition of polymycin B. Stimulation of PAI production by TNF or IL-1 was observed after 2 h and sustained for at least 24 h. Separate addition of TNF or IL-1 gave similar maximal stimulation of PAI production by EC at 500 U/ml and 5 U/ml, respectively, while the addition of both mediators resulted in a 2-fold larger increase. This indicates an additive effect of TNF and IL-1. TNF did not change PAI production by human hepatocytes.To evaluate the effect of TNF in vivo, rats received a bolus injection of 250,000 U TNF/kg. Two h after injection, a 5-fold rise of circulating PAI levels was found (compared to control rats). Thereafter, the levels returned to basal values over a 10 h period. A decrease in circulating white blood cells was observed during the initial 3 h. The number of circulating platelets did not change.We conclude that stimulation of the vascular bed by TNF not only results in a change in surface characteristics of the endothelium, but also can result in systemic changes. The increase in PAI levels by TNF may decrease fibrinolysis.

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