scholarly journals Recombinant human tumor necrosis factor increases mRNA levels and surface expression of HLA-A,B antigens in vascular endothelial cells and dermal fibroblasts in vitro.

1986 ◽  
Vol 83 (2) ◽  
pp. 446-450 ◽  
Author(s):  
T. Collins ◽  
L. A. Lapierre ◽  
W. Fiers ◽  
J. L. Strominger ◽  
J. S. Pober
Anaerobe ◽  
2020 ◽  
Vol 65 ◽  
pp. 102247 ◽  
Author(s):  
Ilya N. Dyakov ◽  
Dilara A. Mavletova ◽  
Irina N. Chernyshova ◽  
Nadezda A. Snegireva ◽  
Marina V. Gavrilova ◽  
...  

1987 ◽  
Vol 166 (5) ◽  
pp. 1390-1404 ◽  
Author(s):  
G Camussi ◽  
F Bussolino ◽  
G Salvidio ◽  
C Baglioni

Murine tumor necrosis factor (mTNF) stimulates production of platelet-activating factor (PAF) by cultured rat peritoneal macrophages in amounts comparable to those formed during treatment with the calcium ionophore A23187 or phagocytosis of zymosan. The cell-associated PAF that was released into the medium was identical to synthetic PAF, as determined with physicochemical, chromatographic, and enzymatic assays. Furthermore, de novo synthesis of PAF by macrophages was demonstrated by the incorporation of radioactive precursors such as [3H]acetyl-coenzyme A or [3H]2-lyso-PAF. Macrophages incubated with mTNF for 4 h synthesized PAF only during the first h of treatment. At this time, the amount of cell-associated PAF was approximately equal to that released into the medium. The cell-associated PAF decreased afterwards, whereas that in the medium did not correspondingly increase, suggesting that some PAF was being degraded. The response of rat macrophages to different doses of mTNF and human TNF (hTNF) was examined. Maximal synthesis of PAF was obtained with 10 ng/ml of mTNF and 50 ng/ml of hTNF. This finding may be explained by a lower affinity of hTNF for TNF receptors of rat cells. The hTNF stimulated production of PAF by human vascular endothelial cells cultured from the umbilical cord vein. The time course of PAF synthesis was slower than that observed with macrophages, with maximal production between 4 and 6 h of treatment. Optimal synthesis of PAF was obtained with 10 ng/ml of hTNF. Only 20-30% of the PAF synthesized by endothelial cells was released into the medium, even after several hours of incubation. Synthesis of PAF in response to TNF was also detected in rat polymorphonuclear neutrophils, but not in human tumor cells and dermal fibroblasts. Therefore, production of PAF is a specialized response that is transient in macrophages continuously treated with TNF, and that appears to be controlled by unidentified regulatory mechanisms.


2001 ◽  
Vol 2 (4) ◽  
pp. 198-201
Author(s):  
Weifen Xie ◽  
Yong Lin ◽  
Xingrong Zhang ◽  
Weizhong Chen ◽  
Xin Zhang ◽  
...  

Blood ◽  
1987 ◽  
Vol 70 (1) ◽  
pp. 200-205
Author(s):  
A Tobler ◽  
D Johnston ◽  
HP Koeffler

Recombinant human tumor necrosis factor alpha (TNF alpha) effectively inhibits clonal growth of leukemic cells from patients and several cell lines, including the promyelocytic HL-60 cells. Decreased expression of the c-myc oncogene is linked to growth arrest and terminal cellular differentiation. The present study characterizes the effect of TNF alpha on the regulation of the c-myc gene in HL-60 cells. TNF alpha (100 U/mL) rapidly inhibited messenger RNA (mRNA) accumulation of c-myc with a 50% reduction in less than one hour. Dose-response studies showed that a 50% reduction of c-myc mRNA occurred in the range of 15 U/mL. In vitro nuclear run-on experiments showed that this decrease of c-myc-mRNA accumulation was the result of a reduced rate of transcription of c-myc by TNF alpha. Further studies demonstrated that TNF alpha did not post-transcriptionally alter levels of c-myc mRNA, and the inhibitory action of TNF alpha on c-myc expression in HL-60 cells did not depend on new protein synthesis. In the conditions of all the experiments, TNF alpha did not affect cell viability. By contrast, TNF alpha (500 U/mL) did not decrease mRNA levels of c-myc in an HL-60 variant cell line whose growth was not inhibited by TNF alpha; also TNF alpha (500 U/mL) increased c-myc-mRNA levels in normal fibroblasts whose growth is known to be stimulated by TNF alpha. These findings, in concert with prior studies, show a close association between growth inhibition of HL-60 cells and decreased levels of mRNA coding for c-myc.


2006 ◽  
Vol 80 (2) ◽  
pp. 162-166 ◽  
Author(s):  
Keisuke Oguma ◽  
Junichi Sano ◽  
Rui Kano ◽  
Toshihiro Watari ◽  
Atsuhiko Hasegawa

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