scholarly journals Plasma levels of tissue-type plasminogen activator and von Willebrand factor in patient with Raynaud's phenomenon

1991 ◽  
Vol 34 (2) ◽  
pp. 255-256 ◽  
Author(s):  
B. Marasini ◽  
M. Cugno ◽  
A. Agostoni
Keyword(s):  
Plasminogen Activator ◽  
Von Willebrand Factor ◽  
Plasma Levels ◽  
Raynaud’S Phenomenon ◽  
Raynaud's Phenomenon ◽  
Tissue Type ◽  
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.

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