scholarly journals Vesicular melatonin efficiently downregulates sodium fluoride-induced rat hepato- and broncho- TNF-α, TGF-β expressions, and associated oxidative injury: a comparative study of liposomal and nanoencapsulated forms

2017 ◽  
Vol Volume 12 ◽  
pp. 4059-4071 ◽  
Author(s):  
Suvomoy Sana ◽  
Swarupa Ghosh ◽  
Nirmalendu Das ◽  
Sibani Sarkar ◽  
Ardhendu Kumar Mandal
Keyword(s):  
Comparative Study ◽  
Sodium Fluoride ◽  
Oxidative Injury ◽  
Tnf Alpha ◽  
Tgf Beta

scholarly journals Tumor necrosis factor alpha is a potent synergistic factor for the proliferation of primitive human hematopoietic progenitor cells and induces resistance to transforming growth factor beta but not to interferon gamma.

1996 ◽  
Vol 183 (2) ◽  
pp. 705-710 ◽  
Author(s):  
H W Snoeck ◽  
S Weekx ◽  
A Moulijn ◽  
F Lardon ◽  
M Lenjou ◽  
...  
Keyword(s):  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Hematopoietic Progenitor Cells ◽  
Tnf Alpha ◽  
Tgf Beta ◽  
Inhibitory Effects ◽  
Hematopoietic Progenitor ◽  
Ifn Gamma ◽  
Kit Ligand ◽  
Necrosis Factor

Since tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and transforming growth factor (TGF)-beta have all been shown to be specific inhibitors of early human hematopoiesis, we wanted to investigate the interactions of these three cytokines on very primitive human adult bone marrow CD34++CD38- hematopoietic progenitor cells, using a pre-colony-forming cell (pre-CFC) assay, which detects the effects of these cytokines on the initial phases of the differentiation of these primitive progenitors, which are unresponsive to interleukin (IL) 3 alone. Surprisingly, TNF-alpha was a very potent stimulator of the proliferation of CD34++CD38- cells and was the most potent synergistic factor for the IL-3-induced proliferation of these cells of all cytokines tested (IL-1, IL-6, granulocyte colony-stimulating factor, kit ligand). TNF-alpha was the only cytokine that, as a single added factor, induced substantial proliferation in CD34++CD38- cells in the presence of IL-3, except for kit ligand, which induced very limited proliferation. TNF-alpha, moreover, induced a high degree of resistance to the inhibitory effects of TGF-beta in a dose-dependent way. The inhibitory effects of IFN-gamma, however, were not affected by the presence of TNF-alpha. We hypothesize that in situations of the hematopoietic stress, TNF-alpha may abrogate the inhibitory effect of ambient TGF-beta in the bone marrow microenvironment to allow primitive stem cells to proliferate and differentiate in response to an increased demand for mature blood cells.

scholarly journals Ability of flt3 ligand to stimulate the in vitro growth of primitive murine hematopoietic progenitors is potently and directly inhibited by transforming growth factor-beta and tumor necrosis factor-alpha

Blood ◽  
1996 ◽  
Vol 87 (12) ◽  
pp. 5016-5026 ◽  
Author(s):  
SE Jacobsen ◽  
OP Veiby ◽  
J Myklebust ◽  
C Okkenhaug ◽  
SD Lyman
Keyword(s):  
Cell Growth ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Tnf Alpha ◽  
Tgf Beta ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Growth Factor Beta ◽  
Necrosis Factor

The recently cloned flt3 ligand (FL) stimulates the growth of primitive hematopoietic progenitor cells through synergistic interactions with multiple other cytokines. The present study is the first demonstrating cytokines capable of inhibiting FL-stimulated hematopoietic cell growth. Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta l) potently inhibited the clonal growth of murine Lin-Sca-l+ bone marrow progenitors stimulated by FL alone or in combination with granulocyte colony-stimulating factor (G-CSF), stem cell factor (SCF), interleukin (IL)-3, IL-6, IL-11, or IL-12. TGF-beta 1 inhibited more than 96% of the myeloid colony formation in response to these cytokine combinations, whereas TNF-alpha reduced the number of colonies by 58% to 96% depending on the cytokine by which FL was combined. In addition, both TNF-alpha and TGF-beta 1 inhibited more than 90% of B220+ cell production from B220- bone marrow cells stimulated by FL + IL-7. The effects of TNF-alpha and TGF-beta 1 appeared to be due to a direct effect and on the early progenitors because the inhibition was observed at the single cell level, and because delayed addition of the two inhibitors for only 48 hours dramatically reduced their inhibitory effects. A neutralizing anti-TGF- beta antibody showed the presence of endogenous TGF-beta in the cultures and potently enhanced the ability of FL to stimulate progenitor cell growth in the absence of other cytokines. Agonistic antibodies specifically activating the p75 TNF receptors were more efficient than wild type murine TNF-alpha in signaling growth inhibition of Lin-Sca-l+ progenitor cells, whereas the p55 agonist had less effect than murine TNF-alpha. Finally, TGF-beta increased the number of FL + IL-11-stimulated Lin-Sca-1+ cells in the G1 phase of the cell cycle with 76%, whereas TNF-alpha only had a marginal effect on cell cycle distribution. Thus, TGF-beta, TNF-alpha, and p75 TNF receptor agonists are potent direct inhibitors of FL-stimulated progenitor cell growth in vitro.

TGF-beta and TNF-alpha producing effects of losartan and amlodipine on human mononuclear cell culture

Nephrology ◽  
2005 ◽  
Vol 10 (5) ◽  
pp. 478-482 ◽  
Author(s):  
KUBRA KAYNAR ◽  
SUKRU ULUSOY ◽  
ERCUMENT OVALI ◽  
BIRGUL VANIZOR ◽  
TAMER DIKMEN ◽  
...  
Keyword(s):  
Cell Culture ◽  
Mononuclear Cell ◽  
Tnf Alpha ◽  
Tgf Beta ◽  
Human Mononuclear Cell ◽  
Mononuclear Cell Culture

Effects of TGF-beta and TNF-alpha on procoagulant and fibrinolytic pathways of human tracheal epithelial cells

1994 ◽  
Vol 267 (6) ◽  
pp. L693-L703 ◽  
Author(s):  
S. Idell ◽  
A. Kumar ◽  
C. Zwieb ◽  
D. Holiday ◽  
K. B. Koenig ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Transforming Growth Factor ◽  
Tnf Alpha ◽  
Tgf Beta ◽  
Tracheal Epithelial Cells ◽  
Fibrin Formation ◽  
Tracheal Epithelial ◽  
Pai 1

The epithelial lining of the airways is subject to injury through several processes, including infections, bronchiolitis, and fume exposures. Because airway fibrin deposition influences the course of local injury, we examined how two inflammatory cytokines influenced fibrin formation and clearance in human tracheal epithelial cells (TEC). TEC were treated with transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha). TNF-alpha increased release of tissue factor (TF)-related procoagulant activity that, through generation of factor Xa, promotes assembly of the prothrombinase complex at the cell surface. Fibrinolytic activity was plasminogen dependent and due to both urokinase (uPA) and tissue plasminogen activator (tPA). The cells expressed plasminogen activator inhibitor 1 (PAI-1), but relatively little PAI-2. Depression of fibrinolysis by TGF-beta correlated with increased PAI-1. Conversely, TNF-alpha increased plasminogen activator (PA) activity due to increased uPA. Fibrinolytic activity was inhibited by actinomycin D and cyclohexamide, but changes in mRNAs for uPA, tPA, PAI-1, and TF by either cytokine were not appreciable. PAI-2 mRNA was not found. The data indicate that TGF-beta decreases the fibrinolytic capacity of TEC, suggesting that this cytokine promotes fibrin retention. TNF-alpha increases expression of both procoagulant and fibrinolytic activities; this differential regulation could favor both pericellular fibrin formation and dissolution.

Serum TGF-Beta 1 and TNF-Alpha Levels and Cardiac Fibrosis in Experimental Chronic Renal Failure

2005 ◽  
Vol 34 (2) ◽  
pp. 143-152 ◽  
Author(s):  
Alexey V. Fedulov ◽  
T. P. Ses ◽  
N. A. Gavrisheva ◽  
M. G. Rybakova ◽  
J. G. Vassilyeva ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Cardiac Fibrosis ◽  
Tnf Alpha ◽  
Tgf Beta

Polymorphisms in Coagulant and Inflammatory Genes Modify the Phenotype of Severe Hemophilia A and B.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1009-1009 ◽  
Author(s):  
G. Jayandharan ◽  
Mercy Devadharshini ◽  
Auro Viswabandya ◽  
Sukesh C. Nair ◽  
R.V. Shaji ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tissue Factor ◽  
Plasminogen Activator ◽  
Protein C ◽  
Tumor Necrosis ◽  
Hemophilia A ◽  
Tnf Alpha ◽  
Severe Hemophilia ◽  
Tgf Beta ◽  
Necrosis Factor

Abstract Among patients with severe hemophilia (<1% factor level), 10–15% are known to have a clinically mild phenotype. The basis for this phenomenon is unclear. We hypothesized that functionally significant polymorphisms in the coagulant, inflammatory and immunoregulatory genes may affect the phenotype of severe hemophilia. A total 114 patients with hemophilia A (n=95) and hemophilia B (n=19) were studied. All these patients were on minimal on-demand treatment. Patients were evaluated for the frequency and site of hemorrhage. Their clinical and radiological joint scores were documented. They were categorized as ‘mild’ (<1 affected joint and < 5 bleeds in the preceding year, n=15) or ‘severe’ (>1 affected joint and >5bleeds, n=99). Functional polymorphisms in the coagulant system (human platelet alloantigen; tissue factor; fibrinogen; factors II; V; VII; XIIIA; thrombin activable fibrinolysis inhibitor (TAFI); endothelial protein C receptor; endothelial nitric oxide synthase 3; tissue plasminogen activator; plasminogen activator inhibitor; tissue factor pathway inhibitor; protein C and S; thrombomodulin), known procoagulant factors (methylene tetrahydrofolate reductase gene), inflammatory cytokine genes (tumor necrosis factor alpha; transforming growth factor beta; interleukin (IL) 10; IL 6; IL 1beta; IL 1 beta receptor antagonist; tumor necrosis factor beta), immunoregulatory cytokine genes (interferon gamma; HLA B27; FC gamma receptor), MDM2, angiotensin converting enzyme and HFE genes were genotyped. The mean age in the two groups was 18.5 & 14.85, p=0.124. The clinical features showing significant difference are shown in the table. Of the polymorphisms studied, the FVII RQ/QQ (lower levels) (RR-3.99, p=0.022, 95% CI 1.2–13.4), TNF alpha-308AA/AG (pro-inflammatory) (RR-3.4, p=0.037, 95% CI, 1.07–10.7), TGF beta Codon 10 CC/CT (pro-inflammatory) (RR-2.8, p=0.07, 95% CI, 0.91–8.3), have been associated with a severe phenotype while MDM2GG (anti-inflammatory, RR-0.3, p=0.038, 95% CI, 0.1–0.93) was associated with a milder phenotype. We hypothesize that the bleeding frequency in severe hemophilia may be increased due to relatively lower FVII levels and a combination of cytokine driven pro-inflammatory state involving TNF alpha, TGF beta and MDM2 would cause destruction of the cartilage resulting in elaboration of metalloproteinases from chondrocytes leading to the development of arthropathy. Parameter Severe, n=99 Median (Range) Mild, n=15 Median (Range) p Value Number of bleeds /yr 15(3–74) 2(0–5) 0.000 Number of joints /yr 3 (1–6) 1 (0–1) 0.000 Age at first clinical symptom (months) 21(1–300) 60(6–90) 0.056 WFH clinical score 10 (0–27) 4 (0–21) 0.000 Pettersson score 13 (0–57) 6 (0–20) 0.001

Biovailability of fluoride in postmenopausal women: Comparative study between sodium fluoride and disodium monofluorophosphate-calcium carbonate

1992 ◽  
Vol 50 (3) ◽  
pp. 209-213 ◽  
Author(s):  
Frédéric Lioté ◽  
Christophe Bardin ◽  
Amélie Liou ◽  
Agnès Brouard ◽  
Jean-Loup Terrier ◽  
...  
Keyword(s):  
Calcium Carbonate ◽  
Comparative Study ◽  
Postmenopausal Women ◽  
Sodium Fluoride
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