Transforming growth factor-beta protection of cancer cells against tumor necrosis factor cytotoxicity is counteracted by hyaluronidase (review).

1998 ◽  
Author(s):  
N S Chang
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Cancer Cells ◽  
Transforming Growth Factor Beta ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Growth Factor Beta ◽  
Necrosis Factor

scholarly journals Modulation of adipocyte differentiation by tumor necrosis factor and transforming growth factor beta.

1989 ◽  
Vol 108 (3) ◽  
pp. 1105-1113 ◽  
Author(s):  
F M Torti ◽  
S V Torti ◽  
J W Larrick ◽  
G M Ringold
Keyword(s):  
Protein Synthesis ◽  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Transforming Growth Factor Beta ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Tgf Beta ◽  
Necrosis Factor Alpha ◽  
Growth Factor Beta ◽  
Necrosis Factor

Cultured TA1 adipocytes treated with tumor necrosis factor alpha (TNF) lose intracytoplasmic lipid and, over a period of days, come to resemble their predifferentiated progenitors (preadipocytes). To examine the extent to which this phenotypic reversion represents a return to a less differentiated cell, we examined three major characteristics that distinguish preadipocytes from adipocytes: (a) pattern of gene expression; (b) hormonal requirement for accelerated adipogenesis; and (c) pattern of protein synthesis. We found that within hours of TNF addition to adipocytes, mRNAs for genes whose expression is augmented during adipogenesis decreased to predifferentiated levels; in addition, like preadipocytes, TNF-treated adipocytes required exposure to hormones to accelerate adipogenesis. Further, the pattern of protein synthesis seen on polyacrylamide gels reverted to that seen before differentiation. Transforming growth factor-beta (TGF-beta) also caused a rapid decrease in expression of adipose genes when added to fully differentiated cells, an effect that was achieved by treatment with either TGF-beta 1 or TGF-beta 2. These effects were seen in the absence of a demonstrable proliferative response to either TNF or TGF-beta. Thus characteristics that define the "terminally" differentiated state in adipocytes are subject to modulation by environmental influences.

scholarly journals Liver Failure Impairs the Intrahepatic Elimination of Interleukin-6, Tumor Necrosis Factor-Alpha, Hepatocyte Growth Factor, and Transforming Growth Factor-Beta

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Dawid Porowski ◽  
Agnieszka Wirkowska ◽  
Ewa Hryniewiecka ◽  
Janusz Wyzgał ◽  
Marek Pacholczyk ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Transforming Growth Factor Beta ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Growth Factor Beta ◽  
Hepatocyte Growth ◽  
Necrosis Factor

The strategic location of the liver and its metabolic activity make it a key organ regulating homeostasis. Our purpose was to examine its participation in removal of cytokines: interleukin-6 (Il-6), tumor necrosis factor-alpha (TNF-α), hepatocyte growth factor (HGF), and transforming growth factor-beta (TGF-β) from the portal circulation in human. 20 liver donors and 20 patients with end-stage liver failure were included in the study. Their blood was collected during liver transplantation from the portal, hepatic, and peripheral vein, and the hepatic artery and cytokines’ concentrations were determined. Using the results the mathematical model of cytokine elimination by the liver was developed. In donors significantly lower levels of IL-6, TNF-α, HGF, and TGF-βwere detected in portal blood compared to hepatic vein. In patients with cirrhosis there were no significant differences of IL-6, TNF-α, and TGF-βlevels between portal and hepatic veins. Significantly higher level of HGF in hepatic compared to portal vein was observed. In healthy liver elimination of the cytokines prevailed over their synthesis, as reflected by the positive values of the elimination ratios. In the cirrhotic liver elimination ratios of Il-6, HGF, and TGF-βwere negative indicating the prevalence of intrahepatic synthesis of cytokines over their removal.

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