Paradoxical effects of tumour necrosis factor-α on rat granulosa cell DNA synthesis

2002 ◽  
Vol 14 (3) ◽  
pp. 133 ◽  
Author(s):  
Guillermo M. Lanuza ◽  
Patricia E. Saragüeta ◽  
Ursula A. Bussmann ◽  
J. Lino Barañao
Keyword(s):  
Dna Synthesis ◽  
Tumour Necrosis Factor ◽  
Granulosa Cell ◽  
Tumour Necrosis ◽  
Inhibitory Action ◽  
Tumour Necrosis Factor Α ◽  
Inhibitory Effects ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumour necrosis factor- α (TNF-α ) has been proposed as an intraovarian modulator of granulosa cell function. The effect of TNF-α on DNA synthesis in cultured rat granulosa cells was examined. Tumour necrosis factor-α stimulated thymidine incorporation when added in the presence of transforming growth factor-β (TGF-β). In contrast, the co-mitogenic effect of follicle-stimulating hormone (FSH) and TGF-β was inhibited in a dose-dependent manner by TNF-α . Inhibition of FSH-dependent DNA synthesis by TNF-α was also found when cultures were co-stimulated with activin A. The inhibitory action of TNF-α on FSH-treated cultures was not associated with changes in cell viability. The inhibitory effects of TNF-α could not be solely explained by a decrease in cAMP levels, since TNF-α was also able to inhibit the stimulation by dibutyryl-cAMP and TGF-β on granulosa cell DNA synthesis. These results suggest that TNF-α regulation of granulosa cell growth is elicited either independently or downstream from gonadotrophin-induced cAMP production. The actions of TNF-α could be only partially mimicked by a cell-permeable analogue of ceramide, thus indicating that actions of this cytokine can not be fully ascribed to an activation of sphingomyelinase. Data presented here indicate that, in addition to its previously demonstrated inhibitory effects on gonadotrophin-induced cell differentiation, TNF-α may also exert a marked inhibition on hormonally stimulated immature granulosa cell proliferation. In contrast to this inhibitory action, this cytokine could amplify the mitogenic action of putative intraovarian growth regulators such as TGF-β. These observations add further support to the notion that TNF-α plays a physiological role as a paracrine modulator of follicle development and may be also relevant to the alteration of ovarian function during physiopathological processes.

Steroidogenesis, proliferation and apoptosis in bovine granulosa cells: role of tumour necrosis factor-α and its possible signalling mechanisms

2002 ◽  
Vol 14 (3) ◽  
pp. 141 ◽  
Author(s):  
G. Basini ◽  
G. L. Mainardi ◽  
S. Bussolati ◽  
C. Tamanini
Keyword(s):  
Nitric Oxide ◽  
Tumour Necrosis Factor ◽  
Granulosa Cell ◽  
Granulosa Cells ◽  
Tumour Necrosis ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
Proliferation And Apoptosis ◽  
Factor Α ◽  
Necrosis Factor

This study was designed to investigate the presence of bioactive tumour necrosis factor-α (TNF-α) in bovine fluid collected from small (<5 mm) and large (>8 mm) follicles, as well as the production of the cytokine by the granulosa cells collected from the same type of follicles. Moreover, the effectiveness of 10, 1 and 0.1 ng mL-1 of human TNF-α (hTNF-α) in affecting the main parameters of granulosa cell function, progesterone (P4) and oestradiol-17β (E2) production, cell proliferation and apoptosis, was tested. In addition, the study aimed to determine whether the signalling mechanisms of TNF-α in these cells involve cAMP, nitric oxide or prostaglandin E2 (PGE2) and F2α (PGF2α). It emerged that bioactive TNF-α is present in follicular fluid from both types of follicles and can be measured in media conditioned by granulosa cells from large follicles. As for the effects of hTNF-α , it inhibits P4 production in cells from both types of follicles and stimulates E2 output in those from small follicles; it does not affect proliferation, but it stimulates granulosa cell apoptosis. Finally, the effects of hTNF-α on bovine granulosa cells are not mediated by nitric oxide or cAMP, as neither of these substances were affected by treatment with the cytokine; however, in some way, they could be mediated through PGE2 and PGF2α, the production of which was inhibited by TNF-α in cells from small follicles.

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

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.

Post-transcriptional effects of extracellular pH on tumour necrosis factor-α production in RAW 246.7 and J774 A.1 cells

2001 ◽  
Vol 100 (3) ◽  
pp. 259-266 ◽  
Author(s):  
Thomas A. HEMING ◽  
Divina M. TUAZON ◽  
Sanat K. DAVÉ ◽  
Ashok K. CHOPRA ◽  
Johnny W. PETERSON ◽  
...  
Keyword(s):  
Tumour Necrosis Factor ◽  
Cell Lines ◽  
Gene Transcription ◽  
Tumour Necrosis ◽  
Extracellular Ph ◽  
Tumour Necrosis Factor Α ◽  
Tnf Α ◽  
J774 Cells ◽  
Factor Α ◽  
Necrosis Factor

The present studies determined the effects of extracellular pH (pHo) on the production of tumour necrosis factor-α (TNF-α) in the macrophage-like cell lines RAW 246.7 and J774 A.1. The cells were activated with lipopolysaccharide (LPS) at pHo 5.5, 6.5 or 7.4. TNF-α gene transcription was monitored by Northern blot analysis. Synthesis of the cytokine was monitored by ELISA measurements of the TNF-α content of cell-conditioned media (extracellularly released TNF-α) and cell lysates (cytosolic TNF-α). The magnitude of the TNF-α response differed markedly between the two cell lines. RAW cells were more responsive to LPS than were J774 cells. However, the effects of pHo on TNF-α production were similar in the two cell lines. TNF-α gene transcription was insensitive to experimental pHo. The pHo had no effect on the abundance of TNF-α mRNA at 2, 4 or 18 h. Nonetheless, synthesis of TNF-α was affected significantly by pHo. The TNF-α contents of cell-conditioned medium and cell lysate at 18 h were reduced progressively at lower pHo values. The data indicate that pHo alters TNF-α production in RAW and J774 cells at a post-transcriptional level. These findings suggest that pHo influences the phenotypic responses of macrophages to activating stimuli and modifies the role that macrophages play in inflammatory and immune actions.

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