scholarly journals Endothelial hemostatic properties in diffuse toxic goiter

2003 ◽  
Vol 49 (5) ◽  
pp. 39-41
Author(s):  
L. V. Vasina ◽  
V. F. Mitreikin ◽  
N. N. Petrishchev
Keyword(s):  
Tumor Necrosis Factor ◽  
Thyroid Hormones ◽  
Tumor Necrosis ◽  
Vascular Diseases ◽  
Blood Levels ◽  
Toxic Goiter ◽  
Fibrinolytic Potential ◽  
Necrosis Factor ◽  
Pai 1 ◽  
Immunopathological Process

Changes in endothelial functional activity and lesion were studied in 38patients with diffuse toxic goiter (DTG) in the presence of thyrotoxicosis. There was an increase in CD4/CD8 ratios and the count of cells carrying CD+ and HLA-DRA. The blood levels of tumor necrosis factor-a (TNF-a) and IL-8 were also significantly higher in thyrotoxicosis than those at remission. There was a significant correlation between the blood levels of thyroid hormones and the higher blood concentration of PAI-1 and a negative correlation with the content of PAI-1, which is indicative of an increase in the blood fibrinolytic potential. There was a considerable rise in the count of circulating endotheliocytes in hyperthyroidism, which was associated with enhanced endothe- liocytic lesion due to the development of immunopathological changes and to the higher blood levels of thyroid hormones. The changes in the blood levels of t-PA, PAI-1, and circulating endotheliocytes may be used as markers of the severity of endothelial lesion, in characterizing the activity of an immunopathological process, and in predicting the development of vascular diseases in DTG.

Progress of fibrinolysis during tumor necrosis factor infusions in humans. Concomitant increase in tissue-type plasminogen activator, plasminogen activator inhibitor type-1, and fibrin(ogen) degradation products

Blood ◽  
1990 ◽  
Vol 76 (11) ◽  
pp. 2284-2289 ◽  
Author(s):  
VW van Hinsbergh ◽  
KA Bauer ◽  
T Kooistra ◽  
C Kluft ◽  
G Dooijewaard ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Degradation Products ◽  
Tissue Type ◽  
Necrosis Factor ◽  
Pai 1

Abstract Several investigators have reported that tumor necrosis factor (TNF) can alter the production of plasminogen activator type-1 (PAI-1) and plasminogen activators (PAs) by endothelial cells in vitro. We have examined the in vivo effects of recombinant human TNF administration on fibrinolysis as assessed by parameters in plasma during a 24-hour period of continuous TNF infusion to 17 cancer patients with active disease. The plasma levels of PAI activity increased sevenfold after 3 and 24 hours of TNF infusion. This was the result of an increase of PAI- 1 antigen; PAI-2 antigen was not detectable. Plasma concentrations of tissue-type PA (t-PA) antigen increased twofold to fivefold after 3 and 24 hours of TNF infusion, whereas urokinase-type PA antigen levels in plasma remained unaltered. After 3 hours of TNF infusion the plasma levels of alpha 2-antiplasmin were slightly decreased, 5% on average, suggesting that fibrinolysis continued. After 24 hours of TNF infusion a highly significant increase in fibrin- plus fibrinogen-degradation products, and separately of fibrin degradation products and fibrinogen degradation products, was found. This indicates that fibrinolysis persisted, at least partly, in the presence of high levels of PAI activity. Whereas PAI-1 production increased, t-PA production by human endothelial cells in vitro remains unaltered or even decreases on TNF addition. It has been shown previously that TNF infusion in our patients results in thrombin and fibrin generation. Therefore, it is possible that thrombin, not TNF, is the actual stimulus for t-PA production in our patients. We speculate that fibrin is formed during TNF infusions and that plasmin is generated by t-PA action immediately on the initial formation of (soluble) fibrin molecules. Such a process may explain the generation of degradation products of both fibrin and fibrinogen during infusion of TNF in patients.

Polymorphism A36G of the tumor necrosis factor receptor 1 gene is associated with PAI-1 levels in obese women

2007 ◽  
Vol 97 (01) ◽  
pp. 62-66 ◽  
Author(s):  
Alenka Mavri ◽  
Delphine Bastelica ◽  
Marjorie Poggi ◽  
Pierre Morange ◽  
Franck Peiretti ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Plasma Concentrations ◽  
Tumor Necrosis Factor Receptor ◽  
Tnf Receptor ◽  
Obese Women ◽  
The Metabolic Syndrome ◽  
Necrosis Factor ◽  
Pai 1

SummaryThe tumor necrosis factor (TNF) pathway may be implicated in etiopathogenesis of PAI-1 overexpression during obesity. The aim of this study was to investigate the influence of polymorphismA36G of the TNF receptor 1 (TNFRSF1A +36A/G) on plasma concentrations of PAI-1 in 163 obese (31 with the metabolic syndrome, MetS) and 150 lean, healthy women. Genotypic and allele frequencies did not significantly differ between obese and lean subjects. TNFRSF1A genotypes were significantly associated with sTNFR1 plasma levels in obese women only (p<0.01); TNFRSF1A +36G/G obese carriers exhibited higher sTNFR1 and PAI-1 levels than A carriers (p<0.01 and p<0.05, respectively). In obese women, the presence of the MetS significantly potentiated the elevation of sTNFR1 and PAI-1 levels observed in the TNFRSF1A+36G/G carriers. Our results suggest that association between TNFRSF1A +36G/G genotype and the MetS renders obese women more prone to activation of the TNF pathway reflected by high circulating sTNFR1 and PAI-1 levels.

Blood Levels of Tumor Necrosis Factor Alpha and Its Type 2 Receptor Are Elevated in Patients with Boston Type I Keratoprosthesis

2019 ◽  
Vol 44 (6) ◽  
pp. 599-606 ◽  
Author(s):  
Eleftherios I. Paschalis ◽  
Elise V. Taniguchi ◽  
James Chodosh ◽  
Louis R. Pasquale ◽  
Kathryn Colby ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Blood Levels ◽  
Type I ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Boston Type I Keratoprosthesis ◽  
Necrosis Factor

Influence of weight reduction on blood levels of C-reactive protein, tumor necrosis factor-α, interleukin-6, and oxylipins in obese subjects

2016 ◽  
Vol 106 ◽  
pp. 39-49 ◽  
Author(s):  
Katharina Möller ◽  
Annika I. Ostermann ◽  
Katharina Rund ◽  
Stefanie Thoms ◽  
Cornelia Blume ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Blood Levels ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Obese Subjects ◽  
Factor Α ◽  
Necrosis Factor

Induction of PAI-1 expression by tumor necrosis factor α in endothelial cells is mediated by its responsive element located in the 4G/5G site

FEBS Journal ◽  
2005 ◽  
Vol 272 (22) ◽  
pp. 5821-5831 ◽  
Author(s):  
Maria Swiatkowska ◽  
Janusz Szemraj ◽  
Czeslaw S. Cierniewski
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Responsive Element ◽  
Factor Α ◽  
Necrosis Factor ◽  
Pai 1

scholarly journals Tumor necrosis factor induces the production of urokinase-type plasminogen activator by human endothelial cells

Blood ◽  
1990 ◽  
Vol 75 (10) ◽  
pp. 1991-1998 ◽  
Author(s):  
VW van Hinsbergh ◽  
EA van den Berg ◽  
W Fiers ◽  
G Dooijewaard
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Tissue Type ◽  
Human Endothelial Cells ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Necrosis Factor ◽  
Pai 1

Abstract Endothelial cells play an important role in the regulation of fibrinolysis by the production of several key regulatory proteins. The cytokines tumor necrosis factor (TNF), lymphotoxin, and interleukin-1 (IL-1), but not interleukin-6, increase the production of plasminogen activator inhibitor-1 (PAI-1) by endothelial cells, whereas they have no stimulatory effect on the production of tissue-type plasminogen activator (t-PA). Primary cultures of human endothelial cells release very little urokinase-type plasminogen activator (u-PA). We report here that TNF and lymphotoxin induce, in a concentration-dependent way, the production of both cellular and secreted u-PA antigen in primary and subcultured human endothelial cells. The TNF-induced increase was accompanied by a more than 10-fold increase in u-PA mRNA. Upon stimulation of early passage umbilical vein endothelial cells by TNF, u- PA was predominantly secreted at the basolateral side, whereas PAI activity and t-PA were found in more equal amounts at the apical and basolateral sides of the cell monolayers. TNF-stimulated u-PA secretion by subcultured human aorta endothelial cells showed only a marginal polarity. The u-PA antigen was present in a plasmin-activatable form (single chain u-PA) and in a nonactivatable form (probably u-PA: PAI-1 complex). During the induction of u-PA by TNF, the ratio between plasmin-activatable u-PA and total u-PA decreased markedly. This may indicate that TNF also increases the degree of u-PA activation. The parallel induction of the synthesis and secretion of both u-PA and PAI- 1 by endothelial cells adds a new aspect to the alterations of the fibrinolytic system caused by inflammatory mediators. This aspect may be significant for the regulation of cell-associated and interstitial plasminogen activator activity.

The Endotoxin-induced Plasminogen Activator Inhibitor-1 Increase in Rabbits Is Not Tumor Necrosis Factor-α Dependent and Can Occur in the Absence of Interleukin-1β

2002 ◽  
Vol 88 (10) ◽  
pp. 639-643 ◽  
Author(s):  
Ramón Montes ◽  
Pablo Rodríguez-Whilhelmi ◽  
Verónica Hurtado ◽  
Akihiro Matsukawa ◽  
Marta Montes ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Tnf Α ◽  
Factor Α ◽  
Activator Inhibitor ◽  
Necrosis Factor ◽  
Pai 1

SummaryThe plasminogen activator inhibitor-1 (PAI-1)-dependent fibrinolytic inhibition occurring in endotoxemia contributes to disseminated intravascular coagulation (DIC). Previous findings suggest that tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) are responsible for the increase in the level of PAI-1. These observations usually arose from mild endotoxemia models. We analyzed the effect of FR167653, an inhibitor of the TNF-α/IL-1β production, on the PAI-1 levels in rabbits given endotoxin at a dose sufficient to induce DIC: the steep plasma PAI-1 increase was not attenuated by FR167653, in spite of achieving efficient inhibition of the TNF-α production. No IL-1β was detected during endotoxemia. These results suggest that PAI-1 increase might be independent of TNF-α and IL-1β. If these findings applied to humans, therapeutic intervention directing these cytokines would not be useful for the treatment of fibrinolysis in patients with severe sepsis.

Tumor necrosis factor induces the production of urokinase-type plasminogen activator by human endothelial cells

Blood ◽  
1990 ◽  
Vol 75 (10) ◽  
pp. 1991-1998
Author(s):  
VW van Hinsbergh ◽  
EA van den Berg ◽  
W Fiers ◽  
G Dooijewaard
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Tissue Type ◽  
Human Endothelial Cells ◽  
Type Plasminogen Activator ◽  
Urokinase Type Plasminogen Activator ◽  
Necrosis Factor ◽  
Pai 1

Endothelial cells play an important role in the regulation of fibrinolysis by the production of several key regulatory proteins. The cytokines tumor necrosis factor (TNF), lymphotoxin, and interleukin-1 (IL-1), but not interleukin-6, increase the production of plasminogen activator inhibitor-1 (PAI-1) by endothelial cells, whereas they have no stimulatory effect on the production of tissue-type plasminogen activator (t-PA). Primary cultures of human endothelial cells release very little urokinase-type plasminogen activator (u-PA). We report here that TNF and lymphotoxin induce, in a concentration-dependent way, the production of both cellular and secreted u-PA antigen in primary and subcultured human endothelial cells. The TNF-induced increase was accompanied by a more than 10-fold increase in u-PA mRNA. Upon stimulation of early passage umbilical vein endothelial cells by TNF, u- PA was predominantly secreted at the basolateral side, whereas PAI activity and t-PA were found in more equal amounts at the apical and basolateral sides of the cell monolayers. TNF-stimulated u-PA secretion by subcultured human aorta endothelial cells showed only a marginal polarity. The u-PA antigen was present in a plasmin-activatable form (single chain u-PA) and in a nonactivatable form (probably u-PA: PAI-1 complex). During the induction of u-PA by TNF, the ratio between plasmin-activatable u-PA and total u-PA decreased markedly. This may indicate that TNF also increases the degree of u-PA activation. The parallel induction of the synthesis and secretion of both u-PA and PAI- 1 by endothelial cells adds a new aspect to the alterations of the fibrinolytic system caused by inflammatory mediators. This aspect may be significant for the regulation of cell-associated and interstitial plasminogen activator activity.

Modulation of Pro- and Antifibrinolytic Properties of Human Peritoneal Mesothelial Cells by Transforming Growth Factor β1 (TGF- β1), Tumor Necrosis Factor α (TNF-α) and Interleukin β1 (IL-1β)

1998 ◽  
Vol 79 (02) ◽  
pp. 362-370 ◽  
Author(s):  
Anne Elbrecht ◽  
Carsten Schauerte ◽  
Bernd Klosterhalfen ◽  
Baffour Amo-Takyi ◽  
Johanna Gehlen ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tumor Necrosis Factor ◽  
Plasminogen Activator ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Mesothelial Cells ◽  
Tnf Α ◽  
Tgf Β1 ◽  
Necrosis Factor ◽  
Pai 1

SummaryA decreased fibrinolytic activity of serosal surfaces appears to be a major factor in the development of peritoneal fibrous adhesions. Serosal fibrinolysis is regulated by mesothelial release of tissue type plasminogen activator (t-PA) and plasminogen activator inhibitor types 1 and 2 (PAI-1 and PAI-2). We investigated the influence of tumor necrosis factor alpha (TNF-α), transforming growth factor β (TGF- β1) and interleukin 1β (IL-1β) on pro- and antifibrinolytic properties of mesothelial cells (HOMC) using a cell/fibrin clot assay. TGF-β1, TNF-α and IL-1β induced a dose dependent 2.9, 2.3 and 1.9-fold increase of PAI-1 antigen, respectively, whereas t-PA concentrations decreased to one third of the control values. This modified PAI-1/t-PA secretion pattern leads to a significant delay of fibrinolysis. Analysis of m-RNA levels revealed increased PAI-1 m-RNA concentrations after 12 h and decreased m-RNA concentrations for t-PA after 6 h. Serosal hypofibrinolysis during peritonitis may be explained at least in part by cytokine effects which thus may favor adhesion formation.

scholarly journals Blood levels of interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha and cognitive functions in patients with obsessive compulsive disorder

2019 ◽  
Vol 89 ◽  
pp. 61-66 ◽  
Author(s):  
Evrim Özkorumak Karagüzel ◽  
Filiz Civil Arslan ◽  
Emel Korkmaz Uysal ◽  
Selim Demir ◽  
Demet Sağlam Aykut ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Blood Levels ◽  
Interleukin 1 Beta ◽  
Obsessive Compulsive ◽  
Necrosis Factor Alpha ◽  
Compulsive Disorder ◽  
Factor Alpha ◽  
Necrosis Factor
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