Analysis of the structure and function of plasminogen activator inhibitor type 1(PAI-1), employing mutants expressed in escherichia coli

1989 ◽  
Vol 3 ◽  
pp. 38
Author(s):  
Jaap Keijer ◽  
Marijke Linders ◽  
Hartmut Ehrlich ◽  
Raymond Klein Gebbink ◽  
Hans Pannekoek
Keyword(s):  
Escherichia Coli ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Structure And Function ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
And Function ◽  
Activator Inhibitor ◽  
Pai 1

Adiponectin is inversely related to plasminogen activator inhibitor type 1 in patients with stable exertional angina

2004 ◽  
Vol 91 (05) ◽  
pp. 1026-1030 ◽  
Author(s):  
Hidetomo Maruyoshi ◽  
Tohru Funahashi ◽  
Shinzo Miyamoto ◽  
Jun Hokamaki ◽  
Hirofumi Soejima ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Plasma Levels ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor Type ◽  
Exertional Angina ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
Pai 1

SummaryAdipose tissue is a secretory organ producing a variety of bioactive substances, such as adiponectin. Adiponectin has antiatherogenic properties while plasminogen activator inhibitor type 1 (PAI-1) is closely involved in the development of atherosclerosis. The relationship between adiponectin and PAI-1 in patients with coronary artery disease (CAD) has not been clarified. This study examined plasma levels of adiponectin and PAI-1 in 64 patients with stable exertional angina (SEA) and 65 patients with the chest pain syndrome (CPS). Plasma logadiponectin levels were significantly lower in patients with SEA (0.62±0.08 µg/dL) compared to those with CPS (0.86± 0.05 µg/dL) (p<0.0001). The plasma levels of log-PAI-1 were significantly higher in patients with SEA (1.23±0.18 ng/mL) compared to those with CPS (1.15±0.22 ng/mL) (p<0.05). Plasma log-adiponectin levels correlated negatively with diabetes mellitus (DM), body mass index (BMI), log-PAI-1 (r=−0.284, p<0.001), triglyceride (TG), and remnant-like particles cholesterol (RLP-C), and positively with high-density lipoprotein cholesterol (HDL-C) levels. Plasma levels of log-PAI-1 correlated positively with DM, BMI, TG and RLP-C levels, and negatively with HDL-C levels. Multiple logistic regression analysis identified sex, angina pectoris, and PAI-1 as independent determinants of hyperadiponectinemia (p<0.05). Adiponectin is inversely related to PAI-1. DM, BMI, TG, HDL-C, and RLP-C are common mediators between adiponectin and PAI-1, and treatment for common mediators may prevent the development of CAD by reducing PAI-1 and increasing adiponectin levels.

scholarly journals Hepatocyte growth factor stimulates expression of plasminogen activator inhibitor type 1 and tissue factor in HepG2 cells

Blood ◽  
1994 ◽  
Vol 84 (1) ◽  
pp. 151-157 ◽  
Author(s):  
J Wojta ◽  
T Nakamura ◽  
A Fabry ◽  
P Hufnagl ◽  
R Beckmann ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Cell Type ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Hepatocyte Growth ◽  
Activator Inhibitor ◽  
Pai 1

Abstract HGF is a powerful mitogen for both rat and human hepatocytes, epithelial cells and endothelial cells in vitro, and is angiogenic in vivo. It has considerable homology with plasminogen and has been shown to upregulate urokinase-type plasminogen activator (u-PA) in endothelial cells as well as u-PA and its receptor in kidney epithelial cells. In this study, we report that human recombinant HGF stimulates expression of plasminogen activator inhibitor type 1 (PAI-1) and tissue factor (TF) in the human hepatoma cell line HepG2. PAI-1 antigen as determined by a specific enzyme-linked immunosorbent assay increased up to threefold in conditioned media of HepG2. This increase was dose dependent with maximum stimulation achieved with a concentration of 50 ng/mL of hepatocyte growth factor (HGF). PAI-1 antigen also increased up to fourfold in the extracellular matrix in HGF treated HepG2. The production of the PAI-1 binding protein vitronectin (Vn) was not affected by HGF. In contrast, TF activity in HepG2 treated with HGF increased up to twofold. As determined by Northern blotting, PAI-1 and TF-specific mRNA were increased significantly in the presence of HGF, whereas Vn mRNA was not affected. The increase in PAI-1 and TF mRNA was also seen when HepG2 were incubated with HGF in the presence of cycloheximide, thereby indicating that de novo protein synthesis is not required to mediate the effect. u-PA could be detected neither in unstimulated or HGF-stimulated HepG2 cells on the antigen level nor on the mRNA level. In conclusion, our data give evidence that HGF, in addition to its proliferative effect for different cell types, is also involved in the local regulation of fibrinolysis and coagulation. One could speculate that HGF might modulate processes requiring matrix degradation by increasing the expression of the protease u-PA in one cell type and by upregulating the expression of the serine protease inhibitor PAI-1 in a different cell type. Because u-PA has been shown to activate latent HGF to the active form, it could furthermore be speculated that by upregulating PAI-1, which in turn could inhibit u- PA, HGF might regulate its own activation.

Non-muscle α-actinin-4 interacts with plasminogen activator inhibitor type-1 (PAI-1)

2004 ◽  
Vol 385 (9) ◽  
Author(s):  
Ulla Magdolen ◽  
Florian Schroeck ◽  
Sabine Creutzburg ◽  
Manfred Schmitt ◽  
Viktor Magdolen
Keyword(s):  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor Type ◽  
Inhibitor Type ◽  
Activator Inhibitor Type ◽  
Activator Inhibitor ◽  
Pai 1
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