scholarly journals Down-regulation of cyclic-nucleotide phosphodiesterase 3B in 3T3-L1 adipocytes induced by tumour necrosis factor α and cAMP

2000 ◽  
Vol 346 (2) ◽  
pp. 337-343 ◽  
Author(s):  
Tova RAHN LANDSTRÖM ◽  
Jie MEI ◽  
Marie KARLSSON ◽  
Vincent MANGANIELLO ◽  
Eva DEGERMAN
Keyword(s):  
Insulin Resistance ◽  
Tumour Necrosis Factor ◽  
Cyclic Nucleotide ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Down Regulation ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

We have used murine 3T3-L1 cells, which differentiate in culture and acquire morphological and biochemical features of mature adipocytes, as a model for studying the expression of cyclic-nucleotide phosphodiesterase (PDE) 3B activity, protein and mRNA during differentiation and during long-term treatment of the cells with tumour necrosis factor α (TNF-α), a cytokine associated with insulin resistance, and a cAMP analogue, N6,2ʹ-O-dibutyryl cAMP (dbcAMP). PDE3B activity, protein and mRNA could be detected 4 days after the initiation of differentiation of 3T3-L1 preadipocytes. Treatment of 3T3-L1 adipocytes with 10 ng/ml TNF-α for 24 h produced a maximal (50%) decrease in PDE3B activity, protein and mRNA, which was well correlated with both activation of protein kinase A (PKA) and stimulation of lipolysis, presumably reflecting an increase in intracellular cAMP concentration. To investigate the effect of cAMP on PDE3B we treated 3T3-L1 adipocytes with dbcAMP. After 4 h with 0.5 mM dbcAMP, PDE3B activity was decreased by 80%, which was also correlated with a decrease in PDE3B protein and mRNA. This effect was abolished in the presence of N-[2-(bromocinnamylamino)ethyl]-5-isoquinolinesulphonamide] (H-89), a specific PKA inhibitor. We conclude that the lipolytic effect of TNF-α involves the down-regulation of PDE3B, which is associated with increased activation of PKA, presumably owing to increased levels of cAMP. In addition, the PKA activation induced by dbcAMP resulted in the down-regulation of PDE3B. These results, which suggest that PDE3B is a novel target for long-term regulation by TNF-α and cAMP, could contribute to the understanding of the mechanisms of insulin resistance.

Differential effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α, interleukin-6 and corticosterone induced by bacterial lipopolysaccharide in mice

1995 ◽  
Vol 144 (3) ◽  
pp. 457-462 ◽  
Author(s):  
G Haskó ◽  
I J Elenkov ◽  
V Kvetan ◽  
E S Vizi
Keyword(s):  
Tumour Necrosis Factor ◽  
Interleukin 6 ◽  
Plasma Levels ◽  
Tumour Necrosis ◽  
Endotoxin Shock ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Abstract The effect of selective block of α2-adrenoreceptors on plasma levels of tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6) and corticosterone induced by bacterial lipopolysaccharide (LPS) was investigated in mice using ELISA and RIA. It was found that the LPS-induced TNF-α response was significantly blunted in mice pretreated with CH-38083, a novel and highly selective α2-adrenoreceptor antagonist (the α2/α1 ratio is >2000). In contrast, LPS-induced increases in both corticosterone and IL-6 plasma levels were further increased by CH-38083. Since it has recently been shown that the selective block of α2-adrenoreceptors located on noradrenergic axon terminals resulted in an increase in the release of noradrenaline (NA), both in the central and peripheral nervous systems, and, in our experiments, that propranolol prevented the effect of α2-adrenoreceptor blockade on TNF-α plasma levels induced by LPS, it seems likely that the excessive stimulation by NA of β-adrenoreceptors located on cytokine-secreting immune cells is responsible for this action. Since it is generally accepted that increased production of TNF-α is involved in the pathogenesis of inflammation and endotoxin shock on the one hand, and corticosterone and even IL-6 are known to possess anti-inflammatory properties on the other hand, it is suggested that the selective block of α2-adrenoreceptors might be beneficial in the treatment of inflammation and/or endotoxin shock. Journal of Endocrinology (1995) 144, 457–462

Selective down-regulation of T cell- and non-T cell-derived tumour necrosis factor α by thalidomide: comparisons with dexamethasone

1999 ◽  
Vol 68 (2-3) ◽  
pp. 325-332 ◽  
Author(s):  
Tom L Rowland ◽  
Simon M McHugh ◽  
John Deighton ◽  
Pamela W Ewan ◽  
Rebecca J Dearman ◽  
...  
Keyword(s):  
T Cell ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Down Regulation ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Intracellular NAD+ levels are associated with LPS-induced TNF-α release in pro-inflammatory macrophages

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Abbas Jawad Al-Shabany ◽  
Alan John Moody ◽  
Andrew David Foey ◽  
Richard Andrew Billington
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Inflammatory Cytokine ◽  
Bacterial Lipopolysaccharide ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Factor Α ◽  
Inflammatory Macrophages ◽  
Inflammatory Macrophage ◽  
Necrosis Factor

Bacterial lipopolysaccharide induces changes in intracellular NAD+ levels in a pro-inflammatory, but not an anti-inflammatory, macrophage model that are correlated with the release of the pro-inflammatory cytokine tumour necrosis factor-α (TNF-α).

scholarly journals The Influence of Interleukin (IL)-1β and IL-6 and Tumour Necrosis Factor-α on Prostaglandin Secretion from Porcine Myometrium during the First Third of Pregnancy

2010 ◽  
Vol 79 (4) ◽  
pp. 559-569 ◽  
Author(s):  
Barbara Jana ◽  
Marlena Koszykowska ◽  
Aneta Andronowska
Keyword(s):  
Protein Expression ◽  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Uterine Contraction ◽  
Tumour Necrosis Factor Α ◽  
Cytokine Network ◽  
Tnf Α ◽  
Cox 2 ◽  
Factor Α ◽  
Necrosis Factor

The present study was undertaken to determine the effect of interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α) on prostaglandin (PG)F2α and PGE2 secretion as well as cyclooxygenase-2 (COX-2) protein expression in myometrium collected on days 25, 30 and 40 of pregnancy in pigs. Myometrial slices were incubated for 16 h with IL-1β, IL-6 and TNF-α (1 or 10 ng/ml of medium) or two combinations of the three cytokines (1 or 10 ng/ml of each cytokine per combination). We demonstrated the stimulatory effect of IL-1β and IL-6 on PGF2α and PGE2 secretion from myometrium collected on all examined days of pregnancy, excepting of influence of IL-6 on release of PGF2α by tissue from day 30. In turn, TNF-α was able to stimulate only PGE2 secretion by myometrium of 40-day-pregnant gilts. The three cytokines applied in combination augmented release of PGE2 from myometrium collected on days 30 and 40 of pregnancy. Stimulation of PGE2 secretion by cytokines used individually was more frequent than that of PGF2α. Moreover, an enhancement in PGF2α and/or PGE2 release was accompanied by an increase of COX-2 protein expression. Our study shows the ability of cytokines to stimulate PGF2α and PGE2 release by porcine myometrium from the first third of pregnancy. Obtained data suggest that locally PGs produced in myometrium influencing the uterine contraction activity may be important for the maintenance of myometrial quiescence during pregnancy and confirm also that the complex cytokine network is an important regulatory mechanism of PGs production during pregnancy.

Levels of Serum Interleukin (IL)-6, IL-1β, Tumour Necrosis Factor-α and Leptin and Their Correlation in Depression

2007 ◽  
Vol 41 (3) ◽  
pp. 266-273 ◽  
Author(s):  
Kun Yang ◽  
Guangrong Xie ◽  
Zhongxing Zhang ◽  
Changhong Wang ◽  
Wenbo Li ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Tumour Necrosis ◽  
Serum Levels ◽  
Tumour Necrosis Factor Α ◽  
Depressed Patients ◽  
Tnf Α ◽  
Male Patients ◽  
Factor Α ◽  
Normal Controls ◽  
Necrosis Factor

Objective: To investigate the relationship between leptin and cytokines in depressed patients. Methods: Thirty-three unmedicated patients (24 female, nine male) with depressive disorder and 23 healthy controls (16 female, seven male) were assessed for serum levels of interleukin (IL)-6, IL-1β, tumour necrosis factor-α (TNF-α) and leptin. Results: Levels of IL-6 and TNF-α in depressed patients were higher than in normal controls. There were significantly lower leptin levels in depressed patients than in normal controls. There were also significant differences in the leptin levels, being higher in female than in male patients, and in female than in male controls. Conclusions: IL-6 and TNF-α cytokines and leptin are important in the psychoimmunology of depressed patients. There were gender differences in leptin levels in depression.

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