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Journal articles on the topic 'Plasminogen activator inhibitor type I (PAI-1)'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Rossignol, Patrick, Eduardo Anglès-Cano, and Henri Lijnen. "Plasminogen activator inhibitor-1 impairs plasminogen activationmediated vascular smooth muscle cell apoptosis." Thrombosis and Haemostasis 96, no. 11 (2006): 665–70. http://dx.doi.org/10.1160/th06-06-0321.

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SummaryThe role of plasminogen activator inhibitor-1 (PAI-1) in vascular smooth muscle cell (VSMC) apoptosis mediated by plasminogen activation was studied with the use of aorticVSMC derived from mice with deficiency of PAI-1 (PAI-1-/-), tissue-type (t-PA-/-) or urokinase-type (u-PA-/-) plasminogen activator or from wildtype (WT) mice with corresponding genetic background. Plasminogen incubated with confluentVSMC was activated ina concentration-dependent and saturable manner for all four cell types, with maximal activation rates that were comparable for WT,u-PA-/and t-PA-/cells,but about two-f

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2

Zeheb, Ron, Usha M. Rafferty, Miguel A. Rodriguez, Peter Andreasen, and Thomas D. Gelehrter. "Immunoaffinity Purification of HTC Rat Hepatoma Cell Plasminogen Activator-Inhibitor-1." Thrombosis and Haemostasis 58, no. 04 (1987): 1017–23. http://dx.doi.org/10.1055/s-0038-1646047.

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SummaryIncubation of HTC rat hepatoma cells with the synthetic glucocorticoid dexamethasone rapidly inhibits tissue-type plasminogen activator activity by inducing a specific plasminogen activator-inhibitor (PAI-1). Using immobilized polyclonal antibodies raised against HT-1080 human fibrosarcoma PAI-1, we have purified HTC PAI-1 from serum-free medium conditioned by dexamethasone-treated HTC hepatoma cells and shown it to be antigenically related to human PAI-1. Greater than 100-fold purification with greater than 75% yield was achieved in a single step. The purified PAI-1 migrates on SDS-pol

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3

Yasar Yildiz, Songul, Pinar Kuru, Ebru Toksoy Oner, and Mehmet Agirbasli. "Functional Stability of Plasminogen Activator Inhibitor-1." Scientific World Journal 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/858293.

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Plasminogen activator inhibitor-1 (PAI-1) is the main inhibitor of plasminogen activators, such as tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), and a major regulator of the fibrinolytic system. PAI-1 plays a pivotal role in acute thrombotic events such as deep vein thrombosis (DVT) and myocardial infarction (MI). The biological effects of PAI-1 extend far beyond thrombosis including its critical role in fibrotic disorders, atherosclerosis, renal and pulmonary fibrosis, type-2 diabetes, and cancer. The conversion of PAI-1 from the active to the laten

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4

Jørgensen, Maja, Malou Philips, Sixtus Thorsen, Johan Selmer, and Jesper Zeuthen. "Plasminogen Activator Inhibitor-1 Is the Primary Inhibitor of Tissue-Type Plasminogen Activator in Pregnancy Plasma." Thrombosis and Haemostasis 58, no. 03 (1987): 872–78. http://dx.doi.org/10.1055/s-0038-1646006.

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SummaryThe aim of the present work was to clarify to what extent plasminogen activator inhibitor-1 (PAI-1) and plasminogen activator inhibitor-2 (PAI-2) contribute to the increase in plasma inhibition of tissue-type plasminogen activator (t-PA) observed during pregnancy. It was demonstrated that a monoclonal antibody against PAI-1 almost completely quenched inhibition of single-chain t-PA and most of the inhibition of two-chain t-PA in plasma during the third trimester of piegnancy. The remaining inhibition of two-chain t-PA was to a great extent abolished by a PAI-2 antibody. The second order

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5

Ikegami, Masahisa, Tetsuro Nagano, Yasushi Hara, et al. "TISSUE TYPE PLASMINOGEN ACTIVATOR (t-PA) AND PLASMINOGEN ACTIVATOR INHIBITOR (PAI) IN TRANSPLANTED KIDNEYS." Japanese Journal of Urology 86, no. 5 (1995): 991–95. http://dx.doi.org/10.5980/jpnjurol1989.86.991.

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6

Lobov, Sergei, David R. Croucher, Darren N. Saunders, and Marie Ranson. "Plasminogen activator inhibitor type 2 inhibits cell surface associated tissue plasminogen activator in vitro." Thrombosis and Haemostasis 100, no. 08 (2008): 319–29. http://dx.doi.org/10.1160/th08-02-0119.

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SummaryRegulation of cellular plasminogen activation is necessary for maintenance of tissue homeostasis. Despite increasing evidence for co-expression of tissue type plasminogen activator (tPA) and plasminogen activator inhibitor type-2 (PAI-2;SERPINB2) under patho/physiological conditions, the inhibition of cell-bound tPAmediated plasminogen activation by PAI-2 has not been addressed. Here we show that PAI-2 can inhibit cell-bound tPA activity in vitro and thus prevent plasmin formation. We also examined the potential involvement in this inhibition of the annexin II heterotetramer (AIIt), one

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7

Carr, Marcus E., C. Krishnamurti, and B. M. Alving. "Effect of Plasminogen Activator Inhibitor-1 on Tissue-Type Plasminogen Activator-Induced Fibrinolysis." Thrombosis and Haemostasis 67, no. 01 (1992): 106–10. http://dx.doi.org/10.1055/s-0038-1648389.

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SummaryThe effect of fibrin on the interaction of human recombinant single-chain tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) was studied in normal rabbit plasma and in plasma with high levels of native PAI-1. t-PA was added to diluted plasma containing calcium (10 mM) and 125I-fibrinogen at 37° C. Clotting was initiated with human thrombin, and lysis was monitored both turbidimetrically and by release of 125I-fibrin degradation products (fdp). The activity of t-PA (50 IU/ml) was rapidly reduced to 15% of the initial value in plasma containing PAI-1 (23 AU/

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8

Sillen, Machteld, and Paul J. Declerck. "A Narrative Review on Plasminogen Activator Inhibitor-1 and Its (Patho)Physiological Role: To Target or Not to Target?" International Journal of Molecular Sciences 22, no. 5 (2021): 2721. http://dx.doi.org/10.3390/ijms22052721.

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Plasminogen activator inhibitor-1 (PAI-1) is the main physiological inhibitor of plasminogen activators (PAs) and is therefore an important inhibitor of the plasminogen/plasmin system. Being the fast-acting inhibitor of tissue-type PA (tPA), PAI-1 primarily attenuates fibrinolysis. Through inhibition of urokinase-type PA (uPA) and interaction with biological ligands such as vitronectin and cell-surface receptors, the function of PAI-1 extends to pericellular proteolysis, tissue remodeling and other processes including cell migration. This review aims at providing a general overview of the prop

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9

Ozel Demiralp, Duygu, Huseyin Aktas, and Nejat Akar. "The Effect of Plasminogen Activator Inhibitor-1 −675 4G/5G Polymorphism on PAI-1 Gene Expression and Adipocyte Differentiation." Clinical and Applied Thrombosis/Hemostasis 14, no. 4 (2007): 438–46. http://dx.doi.org/10.1177/1076029607305081.

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Obesity is a complex, multifactorial chronic disease frequently associated with cardiovascular risks, hypertriglyceridemia, low high-density lipoprotein-cholesterol, high blood pressure, and the insulin resistance that appears to be central to the pathogenesis of Type II diabetes. Plasminogen activator inhibitor-1 expression induced in differentiating adipose tissue, but its role in adipogenesis and obesity is poorly understood. Circulating plasminogen activator inhibitor-1 levels are elevated at an early stage of impaired glucose tolerance, resulting in diabetes and metabolic syndrome. Plasmi

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10

Masson, C., and E. Angles-Cano. "Kinetic analysis of the interaction between plasminogen activator inhibitor-1 and tissue-type plasminogen activator." Biochemical Journal 256, no. 1 (1988): 237–44. http://dx.doi.org/10.1042/bj2560237.

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The kinetics of inhibition of tissue-type plasminogen activator (t-PA) by the fast-acting plasminogen activator inhibitor-1 (PAI-1) was investigated in homogeneous (plasma) and heterogeneous (solid-phase fibrin) systems by using radioisotopic and spectrophotometric analysis. It is demonstrated that fibrin-bound t-PA is protected from inhibition by PAI-1, whereas t-PA in soluble phase is rapidly inhibited (K1 = 10(7) M-1.s-1) even in the presence of 2 microM-plasminogen. The inhibitor interferes with the binding of t-PA to fibrin in a competitive manner. As a consequence the Kd of t-PA for fibr

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11

Ehrlich, H. J., R. K. Gebbink, K. T. Preissner, et al. "Thrombin neutralizes plasminogen activator inhibitor 1 (PAI-1) that is complexed with vitronectin in the endothelial cell matrix." Journal of Cell Biology 115, no. 6 (1991): 1773–81. http://dx.doi.org/10.1083/jcb.115.6.1773.

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Vitronectin endows plasminogen activator inhibitor 1 (PAI-1), the fast-acting inhibitor of both tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA), with additional thrombin inhibitory properties. In view of the apparent association between PAI-1 and vitronectin in the endothelial cell matrix (ECM), we analyzed the interaction between PAI-1 and thrombin in this environment. Upon incubating 125I-labeled alpha-thrombin with endothelial cell matrix (ECM), the protease formed SDS-stable complexes exclusively with PAI-1, with subsequent release of these complexe

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12

Estellés, Amparo, Juan Gilabert, Cristina Andrés, Francisco España, and Justo Aznar. "Plasminogen Activator Inhibitors Type 1 and Type 2 and Plasminogen Activators in Amniotic Fluid during Pregnancy." Thrombosis and Haemostasis 64, no. 02 (1990): 281–85. http://dx.doi.org/10.1055/s-0038-1647301.

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SummaryPlasminogen activator inhibitor activity (PAI), PAI-1 and PAI-2 antigen, and other fibrinolytic parameters were evaluated in amniotic fluid during normal pregnancy and compared with that obtained in plasma of pregnant women. The results indicate the presence of both PAI-1 and PAI-2 in amniotic fluid during normal pregnancy. In amniotic fluid, PAI-1 antigen levels increased from 194 ± 109 ng/ml (first trimester) to 640 ± 396 ng/ml (third trimester) and PAI-2 antigen levels increased from 72 ± 57 ng/ml to 173 ± 97 ng/ml. In contrast, a decrease in tissue-type plasminogen activator (t-PA)

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13

Chen, Yabing, Burton E. Sobel, and David J. Schneider. "The effect of plasminogen activator inhibitor type 1 on apoptosis." Thrombosis and Haemostasis 100, no. 12 (2008): 1037–40. http://dx.doi.org/10.1160/th08-04-0234.

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SummaryPlasminogen activator inhibitor type-1 (PAI-1), an inhibitor of plasminogen activators, inhibits formation of plasmin and plasmin-mediated proteolysis. Apoptosis,or programmed cell death, is a potentially important phenomenon in mediating overall cell death. This review focuses on the influence of PAI-1 on apoptosis. Greater expression of PAI-1 has been associated with increased survival of cells and resistance to apoptosis. PAI-1 appears to influence apoptosis by decreasing cell adhesion (anoikis) as well as its effect on intracellular signaling. Mechanisms by which PAI-1 may render a

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14

van Meijer, Marja, Allart Stoop, Annelies Smilde, Klaus T. Preissner, Anton-Jan van Zonneveld, and Hans Pannekoek. "The Composition of Complexes between Plasminogen Activator Inhibitor 1, Vitronectin and either Thrombin or Tissue-type Plasminogen Activator." Thrombosis and Haemostasis 77, no. 03 (1997): 516–21. http://dx.doi.org/10.1055/s-0038-1655999.

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SummaryVitronectin (VN) is an obligatory cofactor for the inhibition of thrombin by plasminogen activator inhibitor 1 (PAI-1). It accelerates the rate of association between thrombin and PAI-1 more than two orders of magnitude. In contrast, VN does not accelerate the association between tissue-type plasminogen activator (t-PA) and PAI-1. Previously, we reported that the anti-PAI-1 monoclonal antibody (MoAb) CLB-2C8 binds to a short stretch of amino acids of PAI-1, located between residues 128 and 145, and prevents PAI-1 binding to VN. Furthermore, MoAb CLB-2C8 fully blocks the inhibitory activ

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15

Liang, Xiubin, Talerngsak Kanjanabuch, Su-Li Mao, et al. "Plasminogen activator inhibitor-1 modulates adipocyte differentiation." American Journal of Physiology-Endocrinology and Metabolism 290, no. 1 (2006): E103—E113. http://dx.doi.org/10.1152/ajpendo.00605.2004.

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Increased plasminogen activator inhibitor-1 (PAI-1) is linked to obesity and insulin resistance. However, the functional role of PAI-1 in adipocytes is unknown. This study was designed to investigate effects and underlying mechanisms of PAI-1 on glucose uptake in adipocytes and on adipocyte differentiation. Using primary cultured adipocytes from PAI-1+/+ and PAI-1−/− mice, we found that PAI-1 deficiency promoted adipocyte differentiation, enhanced basal and insulin-stimulated glucose uptake, and protected against tumor necrosis factor-α-induced adipocyte dedifferentiation and insulin resistanc

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16

Sillen, Machteld, Stephen D. Weeks, Sergei V. Strelkov, and Paul J. Declerck. "Structural Insights into the Mechanism of a Nanobody That Stabilizes PAI-1 and Modulates Its Activity." International Journal of Molecular Sciences 21, no. 16 (2020): 5859. http://dx.doi.org/10.3390/ijms21165859.

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Plasminogen activator inhibitor-1 (PAI-1) is the main physiological inhibitor of tissue-type (tPA) and urokinase-type (uPA) plasminogen activators (PAs). Apart from being critically involved in fibrinolysis and wound healing, emerging evidence indicates that PAI-1 plays an important role in many diseases, including cardiovascular disease, tissue fibrosis, and cancer. Targeting PAI-1 is therefore a promising therapeutic strategy in PAI-1 related pathologies. Despite ongoing efforts no PAI-1 inhibitors were approved to date for therapeutic use in humans. A better understanding of the molecular m

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17

Rydzewski, A., H. Kawamura, I. Watanabe, Y. Takada, and A. Takada. "Plasminogen activators and plasminogen activator inhibitor (PAI-1) in type II diabetes mellitus." Fibrinolysis 4, no. 3 (1990): 183–88. http://dx.doi.org/10.1016/s0268-9499(05)80051-7.

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18

Balsara, Rashna D., and Victoria A. Ploplis. "Plasminogen activator inhibitor-1: The double-edged sword in apoptosis." Thrombosis and Haemostasis 100, no. 12 (2008): 1029–36. http://dx.doi.org/10.1160/th08-07-0427.

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SummaryPlasminogen activator inhibitor type-1 (PAI-1) is a multi-functional protein. It is a fast-acting inhibitor of plasminogen activators; urokinase-plasminogen activator and tissue type plasminogen activator, and also plays an important role in regulating cell proliferation, adhesion, migration, and signal transduction pathways.These biological events are important processes during angiogenesis and restenosis. PAI-1 has been shown to regulate proliferation, migration, and apoptosis of vascular smooth muscle cells and endothelial cells.The ability of PAI-1 to regulate cellular proliferation

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19

Urano, Tetsumei, Yuko Suzuki, Takayuki Iwaki, Hideto Sano, Naoki Honkura, and Francis J. Castellino. "Recognition of Plasminogen Activator Inhibitor Type 1 as the Primary Regulator of Fibrinolysis." Current Drug Targets 20, no. 16 (2019): 1695–701. http://dx.doi.org/10.2174/1389450120666190715102510.

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The fibrinolytic system consists of a balance between rates of plasminogen activation and fibrin degradation, both of which are finely regulated by spatio-temporal mechanisms. Three distinct inhibitors of the fibrinolytic system that differently regulate these two steps are plasminogen activator inhibitor type-1 (PAI-1), &#945;2-antiplasmin, and thrombin activatable fibrinolysis inhibitor (TAFI). In this review, we focus on the mechanisms by which PAI-1 governs total fibrinolytic activity to provide its essential role in many hemostatic disorders, including fibrinolytic shutdown after trau

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Sen, Prosenjit, Andrey Komissarov, Usha R. Pendurthi, Steven Idell, and L. Vijaya Mohan Rao. "Plasminogen Activator Inhibitor-1 Inhibits Factor VIIa Bound to Tissue Factor." Blood 112, no. 11 (2008): 1023. http://dx.doi.org/10.1182/blood.v112.11.1023.1023.

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Abstract The tissue factor (TF) pathway of coagulation plays a primary role in hemostasis but the aberrant activation of TF-mediated coagulation leads to thrombus formation, the precipitating event in acute myocardial infarction, unstable angina and ischemic stroke. Tissue factor-mediated coagulation also contributes to the pathogenesis of acute lung injury by generating extravascular fibrin deposition in lung parenchyma. Pleural fibrin deposition is a common complication of pleural inflammation and occurs in a wide variety of pleural diseases. Thus, a proper regulation of TF activity is criti

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Fujii, Satoshi, Charles L. Lucore, William E. Hopkins, Joseph J. Billadello, and Burton E. Sobel. "Induction of Synthesis of Plasminogen Activator Inhibitor Type-1 byTissue-Type Plasminogen Activator in Human Hepatic and Endothelial Cells." Thrombosis and Haemostasis 64, no. 03 (1990): 412–19. http://dx.doi.org/10.1055/s-0038-1647329.

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SummaryPlasminogen activator inhibitor type-1 (PAI-1) can modify fibrinolytic activity in vitro and in vivo. The present study was performed to determine whether pharmacologic concentrations of tissue-typeplasminogen activator (t-PA) can initiate negative feedback by stimulating PAI-1 synthesis. In both human hepatoma cells (Hep G2) and human umbilical vein endothelial cells (HUVEC), t-PA increased the total concentrations and appearance of newly synthesized protein inconditioned media of free PAI-1 and PAI-1 complexed with t-PA in a dose and time dependent fashion judging from results after i

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22

Gaffney, Patrick J., and Tracey A. Edgell. "The International Standard for Plasminogen Activator Inhibitor-1 (PAI-1) Activity." Thrombosis and Haemostasis 76, no. 01 (1996): 080–83. http://dx.doi.org/10.1055/s-0038-1650526.

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SummarySince the finding that plasminogen activator inhibitor-1 (PAI-1) may influence the initiation and progression of acute myocardial infarction, the assay of PAI-1 in plasma using a variety of commercial kits has become commonplace. The need for a standard to define the activity of PAI-1 prompted an international collaborative study (ICS) to calibrate the functional potency of a lyophilised plasma PAI-1 preparation (92/654). Since PAI-1 inhibits the 2 major plasminogen activators, tissue-type plasminogen activator (t-PA) and urinary-type plasminogen activator (u-PA) in an equimolar manner

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23

Fortenberry, Yolanda, and Jared Damare. "Inactivation of Plasminogen Activator Inhibitor-1 by RNA Aptamer Molecules." Blood 120, no. 21 (2012): 1107. http://dx.doi.org/10.1182/blood.v120.21.1107.1107.

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Abstract Abstract 1107 Introduction: The serine protease inhibitor (serpin) plasminogen activator inhibitor-1 (PAI-1), binds and inhibits the following plasminogen activators: tissue-type plasminogen activator (tPA), and urokinase-type plasminogen activator (uPA). This decreases plasmin production and triggers the dissolution of fibrin clots. Elevated levels of PAI-1 have been correlated with an increased risk for cardiovascular disease, as well as obesity and metabolic syndrome. Consequently, pharmacologically suppressing PAI-1 might prevent, or successfully treat vascular disease. Several PA

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Jendroszek, Agnieszka, Malene S. Sønnichsen, Andrés C. Muñoz, et al. "Latency transition of plasminogen activator inhibitor type 1 is evolutionarily conserved." Thrombosis and Haemostasis 117, no. 09 (2017): 1688–99. http://dx.doi.org/10.1160/th17-02-0102.

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SummaryPlasminogen activator inhibitor type 1 (PAI-1) is a central regulator of fibrinolysis and tissue remodelling. PAI-1 belongs to the serpin super-family and unlike other inhibitory serpins undergoes a spontaneous inactivation process under physiological conditions, termed latency transition. During latency transition the solvent exposed reactive centre loop is inserted into the central β–sheet A of the molecule, and is no longer accessible to reaction with the protease. More than three decades of research on mammalian PAI-1 has not been able to clarify the evolutionary advantage and physi

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Kuiper, J., M. Otter, A. H. Voorschuur, A. J. van Zonneveld, D. C. Rijken, and Th J. C. van Berkel. "Characterization of the Interaction of a Complex of Tissue-type Plasminogen Activator and Plasminogen Activator Inhibitor Type 1 with Rat Liver Cells." Thrombosis and Haemostasis 74, no. 05 (1995): 1298–304. http://dx.doi.org/10.1055/s-0038-1649930.

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SummaryThe present study was undertaken in order to determine the recognition site for tissue-type plasminogen activator-plasminogen activator inhibitor type 1 [t-PA-PAI-1] complexes in rat liver in vivo and in vitro. After intravenous injection into rats t-PA-PAI-1 complexes were rapidly removed from the plasma and the liver took up 80% of the injected dose. Within the liver parenchymal and endothelial liver cells contributed mainly to the uptake of t-PA-PAI-1, and were responsible for 62% and 24% of the liver uptake, respectively. The interaction of t-PA- PAI-1 with isolated rat parenchymal

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Rømer, Maria, and Ulrik A. Lademann. "Regulation of programmed cell death by plasminogen activator inhibitor type 1 (PAI-1)." Thrombosis and Haemostasis 100, no. 12 (2008): 1041–46. http://dx.doi.org/10.1160/th08-04-0266.

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SummaryElevated levels of plasminogen activator inhibitor-1 (PAI-1) are associated with poor prognosis in cancer. An explanation to the elevated levels of PAI-1 could be a protective response to the increased proteolytic activity, caused by elevated levels of urokinase-type plasminogen activator (uPA) observed in tumours; however, several lines of evidence suggest that PAI-1 may contribute directly to the pathology of the disease. PAI-1 has been reported to have an effect on most of the basic cellular processes including cell adhesion, cell migration, cell invasion, and cell proliferation and

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Camani, Chantal, Olivier Gavin, and Egbert Kruithof. "Cellular Degradation of Free and Inhibitor-bound Tissue-type Plasminogen Activator." Thrombosis and Haemostasis 83, no. 02 (2000): 290–96. http://dx.doi.org/10.1055/s-0037-1613801.

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SummaryThe low density lipoprotein receptor-related protein (LRP) is a multiligand clearance receptor that removes free tissue-type plasminogen activator (t-PA) or complexes of t-PA with plasminogen activator inhibitor type 1 (PAI-1) from the blood circulation or the pericellular space. Co-receptors are essential for LRP-mediated clearance of several ligands (e.g. glycosaminoglycans for thrombin/protease nexin and lipoprotein lipase, and the urokinase receptor for urokinase/PAI-1 complexes). The present study was undertaken to investigate whether LRP-mediated t-PA clearance requires a co-recep

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Seki, Taiichiro, Hideo Imai, Shigeyuki Uno, Toyohiko Ariga, and Thomas D. Gelehrter. "Production of Tissue-Type Plasminogen Activator (t-PA) and Type-1 Plasminogen Activator Inhibitor (PAI-1) in Mildly Cirrhotic Rat Liver." Thrombosis and Haemostasis 75, no. 05 (1996): 801–7. http://dx.doi.org/10.1055/s-0038-1650370.

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SummaryWe have studied the production of tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1) in liver of normal rats and in rats with mild cirrhosis induced by carbon tetrachloride inhalation, to demonstrate the production of these fibrinolytic components and their pathophysiologic role in the liver in vivo. Immunohistochemical study of paraffin-embedded liver sections and fibrin autography of frozen sections showed that the normal rat liver produces very little t-PA or PAI-1. On the contrary, striking t-PA activity and both t-PA and PAI-1 antigens were

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Piarulli, Francesco, Giovanni Sartore, Ciro Rossetti, et al. "Peripheral artery disease in type 2 diabetes: the role of fibrinolysis." Thrombosis and Haemostasis 89, no. 01 (2003): 91–96. http://dx.doi.org/10.1055/s-0037-1613547.

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SummaryThe aim of the present study is to verify the relationship between peripheral artery disease (PAD) and some coagulation/fibrinolysis parameters in type 2 diabetic patients.Sixty-three type 2 diabetic patients, without PAD, were studied at baseline and after 4 years. Assessments included tissue-Plasminogen Activator (t-PA), Plasminogen Activator Inhibitor-1 antigen (PAI-1 Ag), Plasminogen Activator Inhibitor-1 activity (PAI-1 Act), Plasminogen (Pl), Fibrin peptide A (FPA), Fibrinogen (Fr), and the ankle/brachial pressure index (ABI).We observed a significant difference between diabetic p

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Carmeliet, Peter, Jean-Marie Stassen, Ilse Van Vlaenderen, Robert S. Meidell, Désiré Collen, and Robert D. Gerard. "Adenovirus-Mediated Transfer of Tissue-Type Plasminogen Activator Augments Thrombolysis in Tissue-Type Plasminogen Activator–Deficient and Plasminogen Activator Inhibitor-1–Overexpressing Mice." Blood 90, no. 4 (1997): 1527–34. http://dx.doi.org/10.1182/blood.v90.4.1527.

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AbstractImpaired fibrinolysis, resulting from increased plasminogen activator inhibitor-1 (PAI-1) or reduced tissue-type plasminogen activator (t-PA) plasma levels, may predispose the individual to subacute thrombosis in sepsis and inflammation. The objective of these studies was to show that adenovirus-mediated gene transfer could increase systemic plasma t-PA levels and thrombolytic capacity in animal model systems. Recombinant adenovirus vectors were constructed that express either human wild type or PAI-1–resistant t-PA from the cytomegalovirus (CMV) promoter. Both t-PA-deficient (t-PA−/−)

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Carmeliet, Peter, Jean-Marie Stassen, Ilse Van Vlaenderen, Robert S. Meidell, Désiré Collen, and Robert D. Gerard. "Adenovirus-Mediated Transfer of Tissue-Type Plasminogen Activator Augments Thrombolysis in Tissue-Type Plasminogen Activator–Deficient and Plasminogen Activator Inhibitor-1–Overexpressing Mice." Blood 90, no. 4 (1997): 1527–34. http://dx.doi.org/10.1182/blood.v90.4.1527.1527_1527_1534.

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Impaired fibrinolysis, resulting from increased plasminogen activator inhibitor-1 (PAI-1) or reduced tissue-type plasminogen activator (t-PA) plasma levels, may predispose the individual to subacute thrombosis in sepsis and inflammation. The objective of these studies was to show that adenovirus-mediated gene transfer could increase systemic plasma t-PA levels and thrombolytic capacity in animal model systems. Recombinant adenovirus vectors were constructed that express either human wild type or PAI-1–resistant t-PA from the cytomegalovirus (CMV) promoter. Both t-PA-deficient (t-PA−/−) and PAI

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Sahay, Shikha, Madhu Jain, D. Dash, Lavina Choubey, Shuchi Jain, and T. B. Singh. "Role of plasminogen activator inhibitor type 1 (PAI-1) in PCOS patient." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 6, no. 9 (2017): 4052. http://dx.doi.org/10.18203/2320-1770.ijrcog20174061.

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Background: There has been few studies done demonstrating elevated level of PAI-1 in women with Polycystic Ovarian Syndrome (PCOS). PAI-1 has been associated with insulin resistance, obesity, anovulatory infertility, increased risk of cardiovascular disease in PCOS patient. The objective of the study was to find out the plasma level of PAI-1 in PCOS and compare with healthy age matched control. To correlate PAI-1 with various demographic, anthropometric, biochemical and hormonal parameters in PCOS patient and specific relation of PAI-1 with the insulin resistance, obesity, hyperandrogenemia.Me

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HU, ZHAO-YUAN, YI-XUN LIU, KUI LIU, et al. "Expression of tissue type and urokinase type plasminogen activators as well as plasminogen activator inhibitor type-1 and type-2 in human and rhesus monkey placenta." Journal of Anatomy 194, no. 2 (1999): 183–95. http://dx.doi.org/10.1017/s0021878298004506.

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The distribution of mRNAs and antigens of tissue type (t) and urokinase type (u) plasminogen activators (PA) plus their corresponding inhibitors, type-1 (PAI-1) and type-2 (PAI-2) were studied in human and rhesus monkey placentae by in situ hybridisation and immunocytochemistry. Specific monkey cRNA and antibodies against human tPA, uPA, PAI-1 and PAI-2 were used as probes. The following results were obtained. (1) All the molecules tPA, uPA, PAI-1 and PAI-2 and their mRNAs were identified in the majority of the extravillous cytotrophoblast cells of the decidual layer between Rohr's and Nitabuc

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Medcalf, R. L., E. Van den Berg, and W. D. Schleuning. "Glucocorticoid-modulated gene expression of tissue- and urinary-type plasminogen activator and plasminogen activator inhibitor 1 and 2." Journal of Cell Biology 106, no. 3 (1988): 971–78. http://dx.doi.org/10.1083/jcb.106.3.971.

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Constitutive gene expression of four components of plasminogen activating enzyme system, urinary and tissue-type plasminogen activator (u-PA and t-PA), plasminogen activator inhibitor 1 (PAI-1) and PAI-2 in HT-1080 human fibrosarcoma cells, was modulated by the synthetic glucocorticoid dexamethasone (Dex, 10(-7) M). More than 90% of u-PA, t-PA and PAI-1 antigen was found in conditioned medium, whereas PAI-2 was mainly cell associated. In 48-h culture supernatants (expressed per 10(6) cells) PAI-1 antigen increased from 350 to 3,300 ng and t-PA from 19 to 38 ng. u-PA and PAI-2 in the same sampl

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Hogg, M. G., C. H. Evans, and T. J. Smith. "Leukoregulin induces plasminogen activator inhibitor type 1 in human orbital fibroblasts." American Journal of Physiology-Cell Physiology 269, no. 2 (1995): C359—C366. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c359.

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Leukoregulin, a 50-kDa T lymphocyte-derived cytokine, influences the synthesis of collagenase, stromelysin-1, collagen, and hyaluronan in human fibroblasts and is thus a determinant of extracellular matrix economy. We studied the effect of leukoregulin on the expression of plasminogen activator inhibitor type 1 (PAI-1) in human orbital and dermal fibroblasts. The lymphokine upregulated 35S-labeled PAI-1 protein expression in orbital fibroblasts in dose-dependent manner. The effect on extracellular matrix-associated PAI-1 evolved over several hours and was maximal at 10 h, when levels were 75-f

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Keijer, J., M. Linders, AJ van Zonneveld, HJ Ehrlich, JP de Boer, and H. Pannekoek. "The interaction of plasminogen activator inhibitor 1 with plasminogen activators (tissue-type and urokinase-type) and fibrin: localization of interaction sites and physiologic relevance." Blood 78, no. 2 (1991): 401–9. http://dx.doi.org/10.1182/blood.v78.2.401.401.

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Abstract Plasminogen activator inhibitor 1 (PAI-1), an essential regulatory protein of the fibrinolytic system, harbors interaction sites for plasminogen activators (tissue-type [t-PA] and urokinase-type [u-PA]) and for fibrin. In this study, anti-PAI-1 monoclonal antibodies (MoAbs) were used to identify interaction sites of PAI-1 with these components. The binding sites of 18 different MoAbs were established and are located on five distinct “linear” areas of PAI-1. MoAbs, binding to two distinct areas of PAI-1, are able to prevent the inhibition of t-PA by PAI-1. In addition, two interaction

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Keijer, J., M. Linders, AJ van Zonneveld, HJ Ehrlich, JP de Boer, and H. Pannekoek. "The interaction of plasminogen activator inhibitor 1 with plasminogen activators (tissue-type and urokinase-type) and fibrin: localization of interaction sites and physiologic relevance." Blood 78, no. 2 (1991): 401–9. http://dx.doi.org/10.1182/blood.v78.2.401.bloodjournal782401.

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Plasminogen activator inhibitor 1 (PAI-1), an essential regulatory protein of the fibrinolytic system, harbors interaction sites for plasminogen activators (tissue-type [t-PA] and urokinase-type [u-PA]) and for fibrin. In this study, anti-PAI-1 monoclonal antibodies (MoAbs) were used to identify interaction sites of PAI-1 with these components. The binding sites of 18 different MoAbs were established and are located on five distinct “linear” areas of PAI-1. MoAbs, binding to two distinct areas of PAI-1, are able to prevent the inhibition of t-PA by PAI-1. In addition, two interaction sites for

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Arroyo De Prada, Nuria, Florian Schroeck, Eva-Kathrin Sinner, et al. "Interaction of plasminogen activator inhibitor type-1 (PAI-1) with vitronectin." European Journal of Biochemistry 269, no. 1 (2002): 184–92. http://dx.doi.org/10.1046/j.0014-2956.2002.02639.x.

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Tashiro, Yoshihiko, Chiemi Nishida, Kaori Sato-Kusubata, et al. "Inhibition of PAI-1 induces neutrophil-driven neoangiogenesis and promotes tissue regeneration via production of angiocrine factors in mice." Blood 119, no. 26 (2012): 6382–93. http://dx.doi.org/10.1182/blood-2011-12-399659.

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Abstract Plasminogen activator inhibitor-1 (PAI-1), an endogenous inhibitor of a major fibrinolytic factor, tissue-type plasminogen activator, can both promote and inhibit angiogenesis. However, the physiologic role and the precise mechanisms underlying the angiogenic effects of PAI-1 remain unclear. In the present study, we report that pharmacologic inhibition of PAI-1 promoted angiogenesis and prevented tissue necrosis in a mouse model of hind-limb ischemia. Improved tissue regeneration was due to an expansion of circulating and tissue-resident granulocyte-1 marker (Gr-1+) neutrophils and to

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Higazi, AA, A. Mazar, J. Wang, et al. "Single-chain urokinase-type plasminogen activator bound to its receptor is relatively resistant to plasminogen activator inhibitor type 1." Blood 87, no. 9 (1996): 3545–49. http://dx.doi.org/10.1182/blood.v87.9.3545.bloodjournal8793545.

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Urokinase-type plasminogen activator (uPA) is synthesized as single- chain protein (scuPA) with little intrinsic activity. scuPA is activated when it is converted to two-chain urokinase (tcuPA) by plasmin or when it binds as a single-chain molecule to its cellular receptor (uPAR). Previous data indicate that complexes between scuPA and its receptor have somewhat higher affinity for plasminogen than does tcuPA. The current study indicates that plasminogen activator activity of scuPA bound to recombinant, soluble uPAR (suPAR) is also fivefold less sensitive to inhibition by plasminogen activator

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Andrew, Angeline S., Linda R. Klei та Aaron Barchowsky. "Nickel requires hypoxia-inducible factor-1α, not redox signaling, to induce plasminogen activator inhibitor-1". American Journal of Physiology-Lung Cellular and Molecular Physiology 281, № 3 (2001): L607—L615. http://dx.doi.org/10.1152/ajplung.2001.281.3.l607.

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Human epidemiological and animal studies have associated inhalation of nickel dusts with an increased incidence of pulmonary fibrosis. At the cellular level, particulate nickel subsulfide inhibits fibrinolysis by transcriptionally inducing expression of plasminogen activator inhibitor (PAI)-1, an inhibitor of the urokinase-type plasminogen activator. Because nickel is known to mimic hypoxia, the present study examined whether nickel transcriptionally activates PAI-1 through the hypoxia-inducible factor (HIF)-1α signaling pathway. The involvement of the NADPH oxidase complex, reactive oxygen sp

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Yamashita, M., D. N. Darlington, E. J. Weeks, R. O. Jones, and D. S. Gann. "Plasminogen activator inhibitor-1 rises after hemorrhage in rats." American Journal of Physiology-Endocrinology and Metabolism 268, no. 6 (1995): E1065—E1069. http://dx.doi.org/10.1152/ajpendo.1995.268.6.e1065.

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Large hemorrhage leads to hypercoagulability, a phenomenon that has never been well explained. Because an elevation of plasminogen activator inhibitor (PAI)-1 increases procoagulant activity, we have determined whether plasma PAI activity and tissue PAI-1 mRNA are elevated after hemorrhage. Sprague-Dawley rats were bled (20 or 15 ml/kg) 4 days after cannulation. Plasma PAI activity was determined by the capacity of plasma to inhibit tissue-type plasminogen activator activity. Changes of PAI-1 mRNA in various tissues were detected by high-performance liquid chromatography after reverse transcri

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Planus, E., G. Barlovatz-Meimon, R. A. Rogers, S. Bonavaud, D. E. Ingber, and N. Wang. "Binding of urokinase to plasminogen activator inhibitor type-1 mediates cell adhesion and spreading." Journal of Cell Science 110, no. 9 (1997): 1091–98. http://dx.doi.org/10.1242/jcs.110.9.1091.

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Urokinase plasminogen activator and its receptor are both found at the surface of the cell membrane in many cell types. The plasminogen activator inhibitor type-1 (PAI-1) is often associated with the extracellular matrix. The spatial localization of these three molecules could account for their involvement in cell adhesion and/or migration. We have shown previously that the urokinase receptor mediates mechanical force transmission across the cell surface to the cytoskeleton. Here we investigated whether immobilized plasminogen activator inhibitor type 1 (PAI-1) could regulate cell spreading an

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Castelló, Remedios, Amparo Estellés, Carlos Vázquez, et al. "Quantitative Real-Time Reverse Transcription-PCR Assay for Urokinase Plasminogen Activator, Plasminogen Activator Inhibitor Type 1, and Tissue Metalloproteinase Inhibitor Type 1 Gene Expressions in Primary Breast Cancer." Clinical Chemistry 48, no. 8 (2002): 1288–95. http://dx.doi.org/10.1093/clinchem/48.8.1288.

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Abstract Background: The plasminogen activation system and matrix metalloproteinases (MMPs) play a key role in the degradation of basement membrane and extracellular matrix in tissue remodeling, cancer cell invasion, and metastasis. Methods: Quantitative real-time reverse-transcription-PCR (RT-PCR) assays were developed to quantify urokinase-type plasminogen activator (uPA), plasminogen activator inhibitor type 1 (PAI-1), and tissue metalloproteinase inhibitor type 1 (TIMP-1) mRNA in 54 breast cancer tissues. Gene fragments were amplified in a LightCycler real-time PCR system using gene-specif

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Dmytryk, V., O. Savchuk, and P. Yakovlev. "Changes in the content of some components of the plasminogen activation system in the plasma of bladder cancer patients." Bulletin of Taras Shevchenko National University of Kyiv. Series: Biology 80, no. 1 (2020): 15–19. http://dx.doi.org/10.17721/1728_2748.2020.80.15-19.

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Bladder cancer (BC) continues to be a disease with a high mortality rate. Bladder cancer is the sixth for men and seventeenth for women in the incidence of malignancy worldwide. The invasion and metastasis of malignant tumors are caused by a sequence of processes, including loss of cell-cell and / or cell-matrix adhesion, proteolysis, and induction of angiogenesis. Different protease systems are involved in these processes, especially during the invasion and development of metastases. One such protease system is a plasminogen activation system or fibrinolysis system. Changes in the balance of

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Chandler, W. L., M. C. Alessi, M. F. Aillaud, P. Henderson, P. Vague, and I. Juhan-Vague. "Clearance of Tissue Plasminogen Activator (TPA) and TPA/Plasminogen Activator Inhibitor Type 1 (PAI-1) Complex." Circulation 96, no. 3 (1997): 761–68. http://dx.doi.org/10.1161/01.cir.96.3.761.

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Jiang, Yu, Guangping Zhang, Dong Yan, Hong Yang, Zuguang Ye, and Tonghui Ma. "Bioactivity-Guided Fractionation of the Traditional Chinese Medicine Resina Draconis Reveals Loureirin B as a PAI-1 Inhibitor." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/9425963.

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Thrombotic diseases have become a global burden due to morbidity, mortality, and disability. Traditional Chinese medicine has been proven effective in removing blood stasis and promoting blood circulation, but the exact mechanisms remain unclear. Plasminogen activator inhibitor-1 (PAI-1) is a natural inhibitor of tissue-type and urokinase-type plasminogen activators. In this study, we screened four fractions of Resina Draconis (a traditional Chinese medicine) extract for PAI-1 inhibitory activity. Bioactivity-guided purification and chromogenic substrate-based assay led to the identification o

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Gross, T. J., R. H. Simon, C. J. Kelly, and R. G. Sitrin. "Rat alveolar epithelial cells concomitantly express plasminogen activator inhibitor-1 and urokinase." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 4 (1991): L286—L295. http://dx.doi.org/10.1152/ajplung.1991.260.4.l286.

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There is considerable evidence to suggest that intra-alveolar plasminogen activation is instrumental in many aspects of inflammatory lung injury and subsequent tissue repair. Rat alveolar epithelial cells produce large quantities of urokinase-type plasminogen activator (uPA) in vitro, and uPA expression is modulated in association with cellular differentiation and exposure to inflammatory mediators. We now report that these cells also secrete heat-stable PA inhibitory activity having the characteristics of PA inhibitor type 1 (PAI-1). In particular, immunoreactive PAI-1 was demonstrable in con

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Renckens, Rosemarijn, Joris J. T. H. Roelofs, Peter I. Bonta, et al. "Plasminogen activator inhibitor type 1 is protective during severe Gram-negative pneumonia." Blood 109, no. 4 (2006): 1593–601. http://dx.doi.org/10.1182/blood-2006-05-025197.

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Abstract Plasminogen activator inhibitor type-1 (PAI-1) levels are consistently elevated in patients with severe pneumonia and sepsis and highly predictive for an unfavorable outcome. In addition, pneumonia is associated with strongly elevated PAI-1 levels in the pulmonary compartment. However, whether PAI-1 causally affects antibacterial host defense in vivo remains unknown. We report here that pneumonia caused by the common respiratory pathogen Klebsiella pneumoniae is associated with local production of PAI-1 in the lungs of wild-type mice. PAI-1 deficiency impaired host defense as reflecte

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Fay, William P., Andrew C. Parker, Lorraine R. Condrey, and Amy D. Shapiro. "Human Plasminogen Activator Inhibitor-1 (PAI-1) Deficiency: Characterization of a Large Kindred With a Null Mutation in the PAI-1 Gene." Blood 90, no. 1 (1997): 204–8. http://dx.doi.org/10.1182/blood.v90.1.204.

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Abstract Plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of tissue- and urokinase-type plasminogen activators, is considered a critical regulator of the fibrinolytic system. We previously reported a child with abnormal bleeding and complete PAI-1 deficiency caused by a frame-shift mutation in exon 4 of the PAI-1 gene. The purpose of this study was to provide genetic and clinical data on the extended pedigree of the original proband to better define the phenotype associated with PAI-1 deficiency. Allele-specific oligonucleotide hybridization was used to genotype individuals, an

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