Imbalance of Plasminogen Activator Inhibitor Type-1 (PAI-1) and Tissue Plasminogen Activator (t-PA) Activity in Patients With Noonan Syndrome

2010 ◽  
Vol 32 (7) ◽  
pp. 532-536 ◽  
Author(s):  
Parth Mehta ◽  
Robert I. Parker
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Noonan Syndrome ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
Pai 1

Tissue plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) in diabetic foot syndrome

2017 ◽  
Vol 62 (1) ◽  
pp. 87-91 ◽  
Author(s):  
Arleta Kulwas ◽  
Beata Lisewska ◽  
Wiesław Jundziłł ◽  
Barbara Ruszkowska ◽  
Wanda Drewniak ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Diabetic Foot ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Plasminogen ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
Pai 1

Physiological testosterone stimulates tissue plasminogen activator and tissue factor pathway inhibitor and inhibits plasminogen activator inhibitor type 1 release in endothelial cellsThis paper is one of a selection of papers in this Special Issue, entitled International Symposium on Recent Advances in Molecular, Clinical, and Social Medicine, and has undergone the Journal's usual peer-review process.

2007 ◽  
Vol 85 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Hong Jin ◽  
Jijin Lin ◽  
Lu Fu ◽  
Yi-Fang Mei ◽  
Geng Peng ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Mrna Levels ◽  
Tissue Plasminogen ◽  
Tissue Factor Pathway ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
Pai 1

There is a striking gender difference in atherosclerotic vascular disease. For decades, testosterone was considered detrimental to the cardiovascular system. Recent studies, however, have presented some alternative results. The aim of this study was to evaluate the effect of testosterone, using physiological and supraphysiological concentrations, on antigen and mRNA levels of tissue plasminogen activator (tPA), plasminogen activator inhibitor type 1 (PAI-1), and tissue factor pathway inhibitor (TFPI) released by human umbilical vein endothelial cells and to investigate the cellular mechanism. Cells within 2–3 passages were cultured in 25 cm2 flasks or plated onto 96-well plates with a density of about 1 × 105 cells/mL as recommended. The cells were incubated in the presence or absence of testosterone (3, 30, 3 × 103, 3 × 104 nmol/L) for 48 h. Levels of tPA, PAI-1, and TFPI antigen were assayed with ELISA kits. Reverse transcriptase PCR was carried out to detect tPA, PAI-1, and TFPI mRNA levels. Cells were incubated in androgen-receptor antagonist (flutamide 10 µmol/L) or aromatase inhibitor (aminoglutethimide 50 µmol/L) for 3 h, and then the experiments were repeated. Testosterone at a physiologic concentration (30 nmol/L) increased the antigen levels of tPA and TFPI significantly (P < 0.05). However, tPA and TFPI levels were markedly reduced (P < 0.05) at a larger dose (3 × 104 nmol/L). On the other hand, PAI-1 antigen levels decreased significantly at the testosterone concentrations ranging from 3 to 3 × 104 nmol/L (P < 0.05). The change in the levels of tPA and TFPI were reflected in the corresponding change in mRNA levels. Flutamide attenuated the effect of testosterone at physiological concentration (30 nmol/L). The results demonstrated that testosterone at physiological concentrations may have a beneficial influence on the haemostatic system through enhancement of anticoagulant activity, resulting from stimulation of TFPI and tPA expression and inhibition of PAI-1 secretion by the endothelium.

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