Subchronic exposure of cardiomyocytes to low concentrations of tumor necrosis factor ? attenuates the positive inotropic response not only to catecholamines but also to cardiac glycosides and high calcium concentrations

1996 ◽  
Vol 156 (2) ◽  
pp. 135-143 ◽  
Author(s):  
Peter Boekstegers ◽  
Iris Kainz ◽  
Wolfgang Giehrl ◽  
Wolfgang Peter ◽  
Karl Werdan
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Cardiac Glycosides ◽  
Inotropic Response ◽  
Subchronic Exposure ◽  
Low Concentrations ◽  
High Calcium ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-dependent production of human immunodeficiency virus 1 in chronically infected HL-60 cells

Blood ◽  
1993 ◽  
Vol 82 (9) ◽  
pp. 2742-2748 ◽  
Author(s):  
K Kitano ◽  
CI Rivas ◽  
GC Baldwin ◽  
JC Vera ◽  
DW Golde
Keyword(s):  
Human Immunodeficiency Virus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Virus Production ◽  
Viral Production ◽  
Low Concentrations ◽  
Immunodeficiency Virus ◽  
Lag Period ◽  
Low Levels ◽  
Necrosis Factor

Abstract Tumor necrosis factor (TNF) may play a central role in proviral activation and release from latency in cells infected with the human immunodeficiency virus (HIV). We studied viral production and its relation to TNF in a HL-60 cell line (J22-HL-60) infected with a monocytotropic strain of HIV-1JR-FL. Viral production was stimulated to similar levels by TNF, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and 1,25-dihydroxyvitamin D3 (1,25[OH]2D3). Production of the virus was not suppressed by 3′-azido-3′-deoxythymidine (AZT), indicating that viral production was not caused by superinfection. Low concentrations of TNF (0.1 ng/mL) induced viral production with a short lag period of 8 hours, and this proviral activation was specifically suppressed by anti- TNF antibodies. However, induction of virus production by 1,25(OH)2D3 showed an extended lag period of 2 to 3 days. The effect of 1,25(OH)2D3 on virus production was also blocked by anti-TNF antibodies, which suggests the direct participation of TNF in this process. TNF accumulated in the culture supernatant of cells stimulated with 1,25(OH)2D3 with a kinetics consistent with its involvement in the action of 1,25(OH)2D3 on viral production. The J22-HL-60 cell line produced low levels of virus when cultured in the absence of an external stimulus; however, this basal viral production was suppressed greater than 80% in the presence of anti-TNF antibodies. Corresponding low levels of TNF were detected in the culture supernatants. Viral production decreased slowly with increasing passage of the cells, and no virus was detected in the supernatants of cells maintained in culture for several months. Concomitantly, TNF was no longer detected in the supernatant of these cells, which suggests that endogenous autocrine production of TNF drives viral production in the unstimulated cells. However, viral production was stimulated in these cells by low concentrations (0.1 ng/mL) of added TNF. These results argue for a central role for TNF in HIV proviral activation in chronically infected myeloid cells.

scholarly journals Stabilization of the bioactivity of tumor necrosis factor by its soluble receptors.

1992 ◽  
Vol 175 (2) ◽  
pp. 323-329 ◽  
Author(s):  
D Aderka ◽  
H Engelmann ◽  
Y Maor ◽  
C Brakebusch ◽  
D Wallach
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Prolonged Treatment ◽  
Tnf Receptors ◽  
Soluble Receptors ◽  
Low Concentrations ◽  
High Concentrations ◽  
Activity Decay ◽  
Necrosis Factor

The receptors for tumor necrosis factor (TNF) exist in cell-associated as well as soluble forms, both binding specifically to TNF. Since the soluble forms of TNF receptors (sTNF-Rs) can compete with the cell-associated TNF receptors for TNF, it was suggested that they function as inhibitors of TNF activity; at high concentrations, the sTNF-Rs indeed inhibit TNF effects. However, we report here that in the presence of low concentrations of the sTNF-Rs, effects of TNF whose induction depend on prolonged treatment with this cytokine are augmented, reflecting an attenuation by the sTNF-Rs of spontaneous TNF activity decay. Evidence that this stabilization of TNF activity by the sTNF-Rs follows from stabilization of TNF structure within the complexes that TNF forms with the sTNF-Rs is presented here, suggesting that the sTNF-Rs can affect TNF activity not only by interfering with its binding to cells but also by stabilizing its structure and preserving its activity, thus augmenting some of its effects.

Tumor necrosis factor-α impairs contraction but not relaxation in carotid arteries from iNOS-deficient mice

2000 ◽  
Vol 279 (5) ◽  
pp. R1558-R1564 ◽  
Author(s):  
Carol A. Gunnett ◽  
Donald D. Heistad ◽  
Angela Loihl ◽  
Frank M. Faraci
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Carotid Arteries ◽  
Contractile Responses ◽  
Low Concentrations ◽  
Tnf Α ◽  
Prostaglandin F ◽  
Factor Α ◽  
Necrosis Factor

We used mice deficient in expression of inducible NO synthase (iNOS −/−) to directly examine the role of iNOS in impaired vasoconstrictor responses following tumor necrosis factor-α (TNF-α). In iNOS +/+ mice, contraction of carotid arteries in response to prostaglandin F2α(PGF2α) was impaired following TNF-α (100 μg/kg ip)( n = 10, P < 0.01). In contrast to responses in wild-type mice, contraction to low concentrations of PGF2αwere normal, but maximum contraction to PGF2αwas impaired in arteries from iNOS −/− mice treated with TNF-α [0.35 ± .0.02 g ( n = 8) following vehicle and 0.25 ± 0.02 g ( n = 7) following TNF-α ( P < 0.05)]. Aminoguanidine, a relatively selective inhibitor of iNOS, partially restored contraction to PGF2αin vessels from iNOS +/+ mice but had no effect in iNOS −/− mice injected with TNF-α, suggesting that a mechanism(s) other than iNOS contributes to impaired responses. In contrast to contractile responses, relaxation of the carotid artery in response to acetylcholine and nitroprusside was not altered following TNF-α in iNOS +/+ or iNOS −/−mice. Responses of carotid arteries from iNOS −/− mice and effects of aminoguanidine suggest that both iNOS-dependent and iNOS-independent mechanisms contribute to impaired contractile responses following TNF-α.

scholarly journals Tumor necrosis factor-dependent production of human immunodeficiency virus 1 in chronically infected HL-60 cells

Blood ◽  
1993 ◽  
Vol 82 (9) ◽  
pp. 2742-2748
Author(s):  
K Kitano ◽  
CI Rivas ◽  
GC Baldwin ◽  
JC Vera ◽  
DW Golde
Keyword(s):  
Human Immunodeficiency Virus ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Virus Production ◽  
Viral Production ◽  
Low Concentrations ◽  
Immunodeficiency Virus ◽  
Lag Period ◽  
Low Levels ◽  
Necrosis Factor

Tumor necrosis factor (TNF) may play a central role in proviral activation and release from latency in cells infected with the human immunodeficiency virus (HIV). We studied viral production and its relation to TNF in a HL-60 cell line (J22-HL-60) infected with a monocytotropic strain of HIV-1JR-FL. Viral production was stimulated to similar levels by TNF, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), and 1,25-dihydroxyvitamin D3 (1,25[OH]2D3). Production of the virus was not suppressed by 3′-azido-3′-deoxythymidine (AZT), indicating that viral production was not caused by superinfection. Low concentrations of TNF (0.1 ng/mL) induced viral production with a short lag period of 8 hours, and this proviral activation was specifically suppressed by anti- TNF antibodies. However, induction of virus production by 1,25(OH)2D3 showed an extended lag period of 2 to 3 days. The effect of 1,25(OH)2D3 on virus production was also blocked by anti-TNF antibodies, which suggests the direct participation of TNF in this process. TNF accumulated in the culture supernatant of cells stimulated with 1,25(OH)2D3 with a kinetics consistent with its involvement in the action of 1,25(OH)2D3 on viral production. The J22-HL-60 cell line produced low levels of virus when cultured in the absence of an external stimulus; however, this basal viral production was suppressed greater than 80% in the presence of anti-TNF antibodies. Corresponding low levels of TNF were detected in the culture supernatants. Viral production decreased slowly with increasing passage of the cells, and no virus was detected in the supernatants of cells maintained in culture for several months. Concomitantly, TNF was no longer detected in the supernatant of these cells, which suggests that endogenous autocrine production of TNF drives viral production in the unstimulated cells. However, viral production was stimulated in these cells by low concentrations (0.1 ng/mL) of added TNF. These results argue for a central role for TNF in HIV proviral activation in chronically infected myeloid cells.

Low concentrations of uncouplers of oxidative phosphorylation prevent inflammatory activation of endothelial cells by tumor necrosis factor

2015 ◽  
Vol 80 (5) ◽  
pp. 610-619 ◽  
Author(s):  
V. P. Romaschenko ◽  
R. A. Zinovkin ◽  
I. I. Galkin ◽  
V. V. Zakharova ◽  
A. A. Panteleeva ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Oxidative Phosphorylation ◽  
Tumor Necrosis ◽  
Low Concentrations ◽  
Inflammatory Activation ◽  
Necrosis Factor
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