scholarly journals The von Willebrand Factor Collagen-Binding Activity, the Concentrations of Tissue-type Plasminogen Activator and Its Inhibitor in Patients with Mechanical Injury

2009 ◽  
Vol 5 (4) ◽  
pp. 21
Author(s):  
P. V. Gromov ◽  
K. G. Shapovalov ◽  
Yu. A. Vitkovsky
Keyword(s):  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Binding Activity ◽  
Mechanical Injury ◽  
Tissue Type ◽  
Collagen Binding ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

The Simultaneous Acute Release of Tissue-Type Plasminogen Activator and von Willebrand Factor in the Perfused Rat Hindleg Region

1990 ◽  
Vol 63 (03) ◽  
pp. 454-458 ◽  
Author(s):  
N Tranquille ◽  
J J Emeis
Keyword(s):  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Time Course ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryIn perfused rat hindlegs, platelet-activating factor and bradyki-nin induced the acute release of both tissue-type plasminogen activator (t-PA) and von Willebrand Factor (vWF). The time course of release was similar for both proteins, and the amounts of t-PA and vWF released under various conditions were closely correlated. Release of both t-PA and vWF required extracellular calcium, and could be induced by the calcium ionophore A-23187. Protein synthesis was not required for release to occur.Phorbol myristate acetate also induced release of t-PA and vWF, though with a different time course; DDAVP was inactive.The results suggest that the release of t-PA, and that of vWF, are closely linked at the cellular level.

The Role of Cyclic Nucleotides in the Release of Tissue-Type Plasminogen Activator and von Willebrand Factor

1993 ◽  
Vol 69 (03) ◽  
pp. 259-261 ◽  
Author(s):  
N Tranquille ◽  
J J Emeis
Keyword(s):  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Cyclic Nucleotides ◽  
Atrial Natriuretic Factor ◽  
Platelet Activating Factor ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe modulation of the induced acute release of tissue-type plasminogen activator (t-PA) and of von Willebrand factor (vWF) by compounds affecting cyclic nucleotide levels was studied, using an isolated rat hindleg perfusion system. Platelet-activating factor (PAF; 5 nM) or bradykinin (0.8 (μM) were used to induce release of t-PA and vWF.The guanylate cyclase activators sodium nitroprusside and atrial natriuretic factor reduced the induced release of t-PA and vWF. Release was not affected by inhibiting nitric oxide production with NG-nitro-L-arginine. The effects of nitroprusside and atrial natriuretic factor could not be reproduced by infusion of 8-bromo-cGMP.The adenylate cyclase activator forskolin had no effect on bradykinin-induced release of t-PA and vWF, reduced PAF-induced t-PA release, but potentiated PAF-induced vWF release. These modulatory effects were only partially mimicked by infusion of 8-bromo-cAMP.None of the compounds tested was able to induce the release of t-PA or of vWF in the absence of stimulation by bradykinin or platelet-activating factor. Cyclic nucleotides can thus modulate, but not induce, the acute release of t-PA and vWF from perfused rat hindlegs.

Adenosine 3’:5’-Cyclic Monophosphate Induces Regulated Secretion of Tissue-Type Plasminogen Activator and von Willebrand Factor from Cultured Human Endothelial Cells

1998 ◽  
Vol 79 (04) ◽  
pp. 853-858 ◽  
Author(s):  
R. J. Hegeman ◽  
van den Eijnden-Schrauwen ◽  
J. J. Emeis
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Regulated Secretion ◽  
Cyclic Monophosphate ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe effect of compounds increasing intracellular adenosine 3’:5’-cyclic monophosphate [cAMP]i levels (prostacyclin, isoproterenol, forskolin, cholera toxin), and of the cAMP analogs 8-bromo-cAMP and dibutyryl-cAMP, on the regulated secretion (acute release) of tissue-type plasminogen activator (tPA) and von Willebrand factor (vWF) was studied in cultured human umbilical vein endothelial cells (HUVEC).Prostacyclin, isoproterenol and forskolin, which increased [cAMP]i in HUVEC, and the cell-permeant cAMP analog 8-bromo-cAMP induced dose- and time-dependent secretion of tPA and vWF. The extent of vWF and tPA release correlated with [cAMP]i, and was increased by the phosphodiesterase inhibitor isobutylmethylxanthine.In contrast to thrombin, the cAMP-elevating agents did not increase the intracellular calcium concentration [Ca2+]i in HUVEC. At sub-maximal concentrations, the effects of thrombin and prostacyclin were additive.Our results show that an increase in [cAMP]i resulted in regulated secretion (acute release) of tPA and vWF from HUVEC, without the concomitant increase in [Ca2+]i which is, in HUVEC, essential for thrombin-induced regulated secretion to occur. cAMP-induced secretion represents a novel mechanism for causing regulated secretion of tPA and vWF from endothelial cells.

On the Role of Calcium in the Acute Release of Tissue-Type Plasminogen Activator and von Willebrand Factor from the Rat Perfused Hindleg Region

1991 ◽  
Vol 66 (04) ◽  
pp. 479-483 ◽  
Author(s):  
N Tranquille ◽  
J J Emeis
Keyword(s):  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Ex Vivo ◽  
Calcium Ionophore ◽  
Tissue Type ◽  
Calmodulin Antagonist ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryThe involvement of calcium in the release of tissue-type plasminogen activator (t-PA) and von Willebrand Factor (vWF) from vascular endothelial cells was studied ex vivo using a rat hindleg perfusion system. By adding either platelet-activating factor or bradykinin to the perfusing Tyrode solution, a rapid release of t-PA and vWF was induced. Extracellular calcium was required for the acute release of both glycoproteins as this release was totally abolished in the presence of EGTA. The calcium ionophore A-23187 induced (Ca-dependently) the release of both proteins, suggesting that Ca-influx was also sufficient to induce release. The absence of an effect of the calcium L-type channel blockers, verapamil and diltiazem, and of the calcium channel agonist BAY K-8644, suggested that endothelial voltage-operated calcium channels were not involved in release. Trifluoperazine, a calmodulin antagonist, significantly inhibited the induced release of t-PA and vWF, while the "intracellular calcium antagonist" TMB-8 had no effect. Lanthanum chloride (200 εM) inhibited the induced release of t-PA but not that of vWF. Our results suggest that Ca2+ influx is essential for the release of t-PA and vWF from the perfused rat hindleg.

Markers of endothelial dysfunction and severity of hypoxaemia in the Eisenmenger syndrome

2005 ◽  
Vol 15 (5) ◽  
pp. 504-513 ◽  
Author(s):  
Rosangela de P. S. Soares ◽  
Nair Y. Maeda ◽  
Sérgio P. Bydlowski ◽  
Antonio Augusto Lopes
Keyword(s):  
Endothelial Dysfunction ◽  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Functional Class ◽  
Tissue Type ◽  
Eisenmenger Syndrome ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Von Willebrand ◽  
Willebrand Factor

Endothelial dysfunction has been reported in hypoxaemic patients with the Eisenmenger syndrome, but a direct correlation between levels of endothelial markers and the severity of hypoxaemia has not been explored. With this in mind, we compared the levels in the plasma of tissue-type plasminogen activator, thrombomodulin, and von Willebrand factor in 25 patients with the Eisenmenger syndrome. They had a median age of 31 years, and were divided into 2 groups according to their recent clinical history. Thus, 18 patients were stable, being in functional class II or III, seen as outpatients, and having peripheral saturations of oxygen of 89 plus or minus 5 percent. In contrast, 7 patients were unstable, showing episodes of symptoms placing them in functional class IV, requiring care in hospital, and manifesting saturations of oxygen of 77 plus or minus 5 percent. We were able to follow 12 patients, 8 who were stable and 4 unstable, for 24 months. At baseline, levels of von Willebrand factor were higher in the unstable patients when compared to those who were stable, at 142 plus or minus 29 and 110 plus or minus 25 units per decilitre, respectively (p equal to 0.013). This correlated positively with oxygen desaturation (p less than 0.020). The structural abnormalities also correlated positively with the magnitude of hypoxaemia (p less than 0.020). Levels remained higher in the unstable patients throughout the period of follow-up (p equal to 0.006). Tissue-type plasminogen activator was also increased, at 14.3 plus or minus 8.4 versus 6.5 plus or minus 2.7 nanograms per millilitre in controls (p less than 0.001), whereas thrombomodulin was decreased, with values of 14.4 versus 34.6 nanograms per millilitre in controls (p for median values of less than 0.001). There was no correlation with saturations of oxygen. We conclude that measurement of von Willebrand factor, as compared with tissue-type plasminogen activator and thrombomodulin, will prove a better marker of endothelial response to hypoxaemia in patients with the Eisenmenger syndrome.

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