scholarly journals Regulation of lipoprotein lipase activity and mRNA content in rat epididymal adipose tissue in vitro by recombinant tumour necrosis factor

1990 ◽  
Vol 269 (1) ◽  
pp. 123-126 ◽  
Author(s):  
A G Mackay ◽  
J D Oliver ◽  
M P Rogers
Keyword(s):  
Adipose Tissue ◽  
Tumour Necrosis Factor ◽  
Lipoprotein Lipase ◽  
Tumour Necrosis ◽  
Epididymal Adipose Tissue ◽  
Mrna Levels ◽  
Isolated Adipocytes ◽  
Necrosis Factor

Tumour necrosis factor (TNF) has previously been shown to decrease lipoprotein lipase (LPL) activity and mRNA levels in 3T3-L1 cells and in adipose tissue from rats and guinea pigs when injected in vivo, but not to alter LPL activity in human adipocytes incubated in vitro. The effect of recombinant human TNF on LPL activity and mRNA levels in rat epididymal adipose tissue incubated in vitro was examined. LPL activity and mRNA levels fell in adipose tissue taken from fed rats and incubated in Krebs-Henseleit bicarbonate medium with glucose. The addition of insulin and dexamethasone prevented these falls. TNF (400 ng/ml) produced a fall of approx. 50% in LPL activity after 2 h of incubation and of approx. 30% in LPL mRNA levels after 3 h. TNF did not decrease LPL activity in isolated adipocytes. These results demonstrate that rat adipose tissue incubated in vitro is responsive to TNF whereas isolated adipocytes are not.

THE IMMUNOSUPPRESSANT STEROID CHOLESTERYLPHOSPHOSERINE INHIBITS TUMOUR NECROSIS FACTOR-α SECRETION IN VITRO AND IN VIVO

Cytokine ◽  
2000 ◽  
Vol 12 (6) ◽  
pp. 770-773 ◽  
Author(s):  
Laura Facci ◽  
Federico Cusinato ◽  
Alessandro Negro ◽  
Giovanni Monastra ◽  
Anna Signorelli ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Enhanced anti-tumour activity of carmustine (BCNU) with tumour necrosis factor in vitro and in vivo

1990 ◽  
Vol 62 (5) ◽  
pp. 776-780 ◽  
Author(s):  
AL Jones ◽  
JL Millar ◽  
BC Millar ◽  
B Powell ◽  
P Selby ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Anti Tumour Activity ◽  
Tumour Activity ◽  
Necrosis Factor

scholarly journals Downregulation of zinc-α2-glycoprotein in adipose tissue and liver of obese ob/ob mice and by tumour necrosis factor-α in adipocytes

2009 ◽  
Vol 204 (2) ◽  
pp. 165-172 ◽  
Author(s):  
T Mracek ◽  
D Gao ◽  
T Tzanavari ◽  
Y Bao ◽  
X Xiao ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Protein Content ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Zucker Rats ◽  
Potential Candidate ◽  
Mrna Levels ◽  
Tumour Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

Zinc-α2-glycoprotein (ZAG, also listed as AZGP1 in the MGI Database), a lipid-mobilising factor, has recently been suggested as a potential candidate in the modulation of body weight. We investigated the effect of increased adiposity on ZAG expression in adipose tissue and the liver and on plasma levels in obese (ob/ob) mice compared with lean siblings. The study also examined the effect of the pro-inflammatory cytokine tumour necrosis factor-α (TNFα) on ZAG expression in adipocytes. Zag mRNA levels were significantly reduced in subcutaneous (fourfold) and epididymal (eightfold) fat of ob/ob mice. Consistently, ZAG protein content was decreased in both fat depots of ob/ob mice. In the liver of obese animals, steatosis was accompanied by the fall of both Zag mRNA (twofold) and ZAG protein content (2.5-fold). Plasma ZAG levels were also decreased in obese mice. In addition, Zag mRNA was reduced in epididymal (fivefold) and retroperitoneal (fivefold) adipose tissue of obese (fa/fa) Zucker rats. In contrast to Zag expression, Tnfα mRNA levels were elevated in adipose tissue (twofold) and the liver (2.5-fold) of ob/ob mice. Treatment with TNFα reduced Zag gene expression in differentiated adipocytes, and this inhibition was chronic, occurring at 24 and 48 h following TNFα treatment. It is concluded that ZAG synthesis in adipose tissue and the liver is downregulated, as are its circulating levels, in ob/ob mice. The reduced ZAG production may advance the susceptibility to lipid accumulation in these tissues in obesity, and this could be at least in part attributable to the inhibitory effect of TNFα.

The effects of tumour necrosis factor on host—parasite relations in murine Mesocestoides corti (Cestoda) infection

Parasitology ◽  
1992 ◽  
Vol 105 (3) ◽  
pp. 453-459 ◽  
Author(s):  
P. Jenkins ◽  
S. Spiers ◽  
J. B. Dixon ◽  
S. D. Carter ◽  
S. May
Keyword(s):  
Tumour Necrosis Factor ◽  
Post Infection ◽  
Tumour Necrosis ◽  
Fold Increase ◽  
Peritoneal Macrophages ◽  
Hepatic Necrosis ◽  
Peritoneal Cells ◽  
Necrosis Factor

SUMMARYThe regulatory role of tumour necrosis factor (TNF) was investigated in murine infection with tetrathyridia of Mesocestoides corti. Recombinant TNFα reduced macrophage larvicidal activity in vitro. M. corti primed mice for TNF release in response to bacterial lipopolysaccharide (LPS) in vivo. TNF activity was amplified 100-fold at 14 days post-infection (p.i.), with a further rise at day 28 p.i. Maximal inflammatory reaction was observed histologically in the liver at the height of TNF activity. Hepatic necrosis was located within inflammatory foci, but not within the vicinity of the parasite itself, suggesting that TNF may contribute to the pathogenesis of infection. Peritoneal cells from infected mice, when stimulated with tetrathyridia in vitro, showed a 4-fold increase in TNFα activity at day 14 p.i. However, when peritoneal cells were stimulated with LPS in vitro, a marked increase in TNFα secretion was observed at 2 months post-infection followed by a slow decline. It is suggested that impaired macrophage effector function, previously attributed to endogenous endotoxin, which gains access to peritoneal macrophages through an inability of the liver to detoxify endotoxin, may be mediated through TNFα.

Anti-Tumour Necrosis Factor-α Treatment Interferes with Changes in Lipid Metabolism in a Tumour Cachexia Model

1994 ◽  
Vol 87 (3) ◽  
pp. 349-355 ◽  
Author(s):  
Neus Carbó ◽  
Paola Costelli ◽  
Luciana Tessitore ◽  
Gregory J. Bagby ◽  
Francisco J. López-Soriano ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Tumour Necrosis Factor ◽  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Lipoprotein Lipase Activity ◽  
Tumour Bearing ◽  
Factor Α ◽  
Necrosis Factor

1. Rats bearing the Yoshida ascites hepatoma AH-130 showed an important decrease in white adipose tissue lipoprotein lipase activity as compared with non-tumour bearing rats. This was associated with a lower adipose tissue mass, as estimated from the weight of the lumbar fat-pads. Conversely, lipoprotein lipase activity was markedly increased in brown adipose tissue and heart. 2. These changes were associated with a distinct hyperlipaemia, essentially manifested as an increase in circulating triacylglycerol levels, whereas no changes were observed in glycaemia. 3. Tumour-bearing rats were treated with a polyclonal anti-murine tumour necrosis factor-α antibody or with a non-immune IgG preparation. Control animals were either untreated or received a nonimmune IgG preparation. Anti-tumour necrosis factor-α treatment resulted in a significant increase in lipoprotein lipase activity in white adipose tissue in animals bearing a tumour growing exponentially (day 4 after inoculation) as compared with the animals receiving a non-immune goat IgG preparation. In addition, animals bearing an stationary tumour (day 7 after inoculation) and submitted to anti-tumour necrosis factor-α treatment had a higher adipose tissue lipoprotein lipase activity as compared with the IgG- or the non-treated groups. Correspondingly, circulating triacylglycerol levels were markedly decreased, with a lower hyperlipaemia than in control tumour-bearing rats. 4. These observations suggest that tumour necrosis factor-α is involved in activating the lipid metabolic changes that develop in rats after transplantation of a fast-growing tumour.

scholarly journals Blocking connexin43 hemichannels protects mice against tumour necrosis factor-induced inflammatory shock

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Tinneke Delvaeye ◽  
Maarten A. J. De Smet ◽  
Stijn Verwaerde ◽  
Elke Decrock ◽  
Aleksandra Czekaj ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Single Channel ◽  
Endothelial Barrier ◽  
Barrier Dysfunction ◽  
Intracellular Ca ◽  
Necrosis Factor

Abstract Upon intravenous injection of tumour necrosis factor (TNF) in mice, a systemic inflammatory response syndrome (SIRS) is initiated, characterized by an acute cytokine storm and induction of vascular hyperpermeability. Connexin43 hemichannels have been implicated in various pathological conditions, e.g. ischemia and inflammation, and can lead to detrimental cellular outcomes. Here, we explored whether targeting connexin43 hemichannels could alleviate TNF-induced endothelial barrier dysfunction and lethality in SIRS. Therefore, we verified whether administration of connexin43-targeting-peptides affected survival, body temperature and vascular permeability in vivo. In vitro, TNF-effects on connexin43 hemichannel function were investigated by single-channel studies and Ca2+-imaging. Blocking connexin43 hemichannels with TAT-Gap19 protected mice against TNF-induced mortality, hypothermia and vascular leakage, while enhancing connexin43 hemichannel function with TAT-CT9 provoked opposite sensitizing effects. In vitro patch-clamp studies revealed that TNF acutely activated connexin43 hemichannel opening in endothelial cells, which was promoted by CT9, and inhibited by Gap19 and intracellular Ca2+-buffering. In vivo experiments aimed at buffering intracellular Ca2+, and pharmacologically targeting Ca2+/calmodulin-dependent protein kinase-II, a known modulator of endothelial barrier integrity, demonstrated their involvement in permeability alterations. Our results demonstrate significant benefits of inhibiting connexin43 hemichannels to counteract TNF-induced SIRS-associated vascular permeability and lethality.

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