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Gene Information
Gene symbol: SERPINE1
Gene name: serpin peptidase inhibitor, clade E (nexin, plasminogen activator inhibitor type 1), member 1
HGNC ID: 8583
Synonyms: PAI
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 3138900 | There were positive and independent correlations between tissue plasminogen activator (tPA) activity after venous occlusion and HbA1c, and between triglycerides and plasminogen activator inhibitor (PAI-1) and tPA antigen concentrations before and after venous occlusion. |
| 2 | 2505017 | The decrease of t-PA activity strongly correlated with greater basal levels of plasminogen activator inhibitor in these same subjects. |
| 3 | 2678583 | Type 2 diabetic patients are known to frequently have a high insulin level and were recently described as having high plasminogen activator inhibitor (PAI) activity, compared to normal controls. |
| 4 | 2678583 | As we have shown in several clinical conditions (normal subjects, obese patients, angina pectoris patients) that plasma PAI activity was linked with plasma insulin, we have studied in 38 type 2 diabetic patients the relationship between PAI activity, insulin and other parameters. |
| 5 | 2678583 | Patients showed higher level of PAI activity, as well as plasma glucose, insulin, triglyceride, cholesterol and Apolipoprotein B levels than normal controls; highest values were observed with diabetic patients also affected by coronary artery disease. |
| 6 | 2678583 | A significant correlation was found between PAI activity and insulin (r = 0.60, p less than 0.001), body mass index (r = 0.32, p less than 0.05) and Apolipoprotein B (r = 0.33, p less than 0.05). |
| 7 | 2147433 | When glycosylated hemoglobin levels were in excess of 10%, the f-tPA activity was significantly decreased, but no reduction was found in PAI activity as compared with controls. |
| 8 | 1702773 | The authors examined the effect of insulin-like growth factor 1 (IGF 1), epidermal growth factor (EGF), and acidic fibroblast growth factor (AFGF) on the synthesis by human retinal endothelial cell (HREC) of plasminogen activators (PA; tissue-type [t-PA] and urokinase-type [u-PA]) and plasminogen activator inhibitor (PAI). |
| 9 | 1902595 | ELT was significantly shortened and tPA was markedly increased after the VOT in all 3 groups whereas PAI had not significantly changed. |
| 10 | 2024072 | However, the lower level of t-PA activity after venous occlusion together with the higher levels of VIII: C, VIII R: Ag, alpha 2PI, PAI-1, and plasmin.alpha 2PI complex before venous occlusion in the patients, indicated that the patient group was in a hypercoagulable and hypofibrinolytic state. |
| 11 | 2070877 | Selective assay methods show that almost invariably the fibrinolytic activity of these patients is depressed either following increased levels of fibrinolytic inhibitors (mainly plasminogen activator inhibitor 1 or PAI-1) and/or decreased levels of a plasminogen activator (tissue plasminogen activator or t-PA). |
| 12 | 1908183 | In Type I diabetic patients, after 2-3 months of treatment with gliclazide, we observed a significant increase in plasma concentrations of total t-PA antigen that remained stable until discontinuation of the drug (p less than 0.0002), whereas the plasma concentrations of plasminogen activator inhibitor (PAI) did not change significantly during the study. |
| 13 | 1908183 | Moreover, the plasma concentrations of total t-PA antigen increased significantly (p less than 0.02) in this group of diabetic patients while PAI remained unchanged. |
| 14 | 1719559 | We hypothesized that insulin and insulin-like growth factor type I (IGF-I) can influence synthesis of PAI-1, thereby potentially attenuating fibrinolysis. |
| 15 | 1719559 | In HepG2 cells used as a model system, concentrations of insulin and IGF-I consistent with those seen in plasma independently stimulated PAI-1 synthesis. |
| 16 | 1719559 | Accumulation of PAI-1 protein in conditioned medium over 24 hr was stimulated more with insulin alone than with the combination. |
| 17 | 1772997 | PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. |
| 18 | 1803511 | Reviewed are studies that indicate that it is possible in patients with diabetes by means of sulfonylurea compounds to increase endothelial cell-produced t-PA without affecting PAI-1. |
| 19 | 1579896 | Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of PAI antigen and activity. |
| 20 | 1612205 | Because increased concentrations of plasminogen activator inhibitor type-1 (PAI-1) occur also, we hypothesized that proinsulin and split proinsulin may augment endothelial cell PAI-1 expression, thereby potentially attenuating endogenous fibrinolysis and accelerating atherosclerosis. |
| 21 | 1612205 | Proinsulin increased PAI-1 activity in conditioned media of endothelial cells as did split proinsulin, paralleled by increased expression of PAI-1 mRNA. |
| 22 | 1612205 | The proinsulin stimulation of PAI-1 expression was not attenuated by either anti-insulin receptor antibodies or a 100-fold excess of insulin. |
| 23 | 1612205 | These results indicate that proinsulin augments PAI-1 expression, potentially contributing to vasculopathy in patients with non-insulin-dependent diabetes mellitus. |
| 24 | 1459169 | The mean plasminogen inhibitor-1 (PAI-1) activity of the patients was elevated compared with healthy controls. |
| 25 | 1459169 | In spite of the reduction of the triglyceride concentrations and unchanged insulin levels, there was a significant increase of the activity of PAI-1 (+21%, P < 0.01) after MaxEPA suggesting a possible impairment of the fibrinolytic capacity. |
| 26 | 1468721 | The coronary patients had significantly higher plasminogen activator inhibitor (PAI) activity than the control subjects, while t-PA antigen did not differ between the groups. |
| 27 | 8420806 | Concordant increases of plasma PAI-1 and plasma IRI appear to reflect direct effects of insulin and proinsulin on the synthesis and secretion of PAI-1 by endothelial and liver cells as judged from results of studies in vitro. |
| 28 | 8443145 | Levels of PAI-1 activity (18.7 +/- 5.6 versus 12.0 +/- 3.8 arbitrary units [AU] per milliliter, p = 0.001) and t-PA antigen (7.0 +/- 1.9 versus 4.6 +/- 2.0 ng/mL, p = 0.001) were significantly higher in diabetic compared with nondiabetic control subjects. |
| 29 | 8443145 | Survivors of myocardial infarction had higher levels of PAI-1 activity and antigen and t-PA antigen than control subjects, and the diabetic survivors had higher levels of PAI-1 activity (25.3 +/- 6.7 versus 20.1 +/- 7.1 AU/mL, p = 0.004) and t-PA antigen (10.6 +/- 4.3 versus 8.4 +/- 3.3 ng/mL, p = 0.03) than the nondiabetic survivors. |
| 30 | 8475477 | Plasminogen activator inhibitor-1 (PAI) activity, plasma insulin, glucose, cholesterol and triglyceride (TG) concentrations were determined in 32 Chinese diabetic patients (mean age 61.4 yr) and 41 healthy controls (mean age 64.5 yr) to establish the relationships between these parameters. |
| 31 | 8475477 | Insulin, glucose, cholesterol and triglyceride levels were significantly higher in the diabetics, whereas no significant difference of PAI activity was noted between groups. |
| 32 | 8475477 | PAI activity was not affected by the increase of plasma insulin, cholesterol, TG or glucose. |
| 33 | 8261243 | To determine whether the increased PAI-1, known to be associated with accelerated coronary artery disease in non-diabetic subjects, is a consequence of direct effects of insulin on endothelial cells, we performed the present study with primary cultures of human aortic endothelial cells. |
| 34 | 8261243 | Insulin at pharmacologic concentrations did not alter either PAI-1 or t-PA production by the human aortic endothelial cells, although insulin stimulated PAI-1 synthesis in human hepatoma (Hep G2) cells as expected. |
| 35 | 8304913 | Although compensatory hyperinsulinaemia may prevent the development of NIDDM in insulin-resistant individuals, there is substantial evidence that insulin resistance and/or hyperinsulinaemia is associated with higher plasma concentrations of triglyceride, uric acid and plasminogen activator inhibitor 1 and with lower HDL cholesterol concentrations. |
| 36 | 8281664 | We and others have hypothesized that the increased PAI-1 may contribute to acceleration of atherosclerosis in this condition and in other states characterized by insulin resistance as well. |
| 37 | 8281664 | To assess this possibility directly, this study was performed to identify potential direct effects of proinsulin and proinsulin split products on synthesis of PAI-1 in liver cells, thought to be the major source of circulating PAI-1 in vivo. |
| 38 | 8281664 | Stimulation was transduced at least in part by the insulin receptor as shown by inhibition of stimulation by insulin receptor antibodies, mediated at the level of PAI-1 gene expression as shown by the 2.2- to 2.9-fold increases in steady-state concentrations of PAI-1 mRNA, and indicative of newly synthesized protein as shown by results in metabolic labeling experiments. |
| 39 | 8281664 | Our results are consistent with the hypothesis that precursors of insulin (proinsulin and proinsulin split products), known to be present in relatively high concentrations in plasma in patients with NIDDM and conditions characterized by insulin resistance, may directly stimulate PAI-1 synthesis, thereby attenuating fibrinolysis and accelerating atherogenesis. |
| 40 | 8120522 | Tissue plasminogen activator antigen measured after venous occlusion showed a significant reduction whilst plasminogen activator inhibitor 1 activity was 26.0 +/- 9.8 IU ml-1 on oral treatment and 18.2 +/- 4.7 IU ml-1 on insulin treatment (NS). |
| 41 | 7519664 | A decrease in the local tissue activity of PAI-1 by elevated glucose concentrations, with no effect on tPA or uPA expression, would lead to an increase in the plasmin activity and thereby predispose neural tissues, such as the cerebrum and retina, of diabetic patients to neovascularization. |
| 42 | 7828304 | To define the possible presence of such an axis, this study was designed to determine whether insulin, its precursors, or both increase the concentrations of PAI-1 in rabbits in vivo. |
| 43 | 7828304 | Plasma PAI-1 activity increased 3.8-fold with proinsulin (P = .002) and 3.6-fold with insulin (P = .002). |
| 44 | 7828304 | As judged from changes in mRNA in tissues, proinsulin and insulin increased PAI-1 gene expression within 3 hours by 2.1- and 2.1-fold, respectively, in aorta (P = .025 each) and by 1.9- and 2.4-fold in liver (P = .015 and P = .001), with return of values to baseline within 24 hours (n = 4 experiments in each case). |
| 45 | 7883982 | These findings suggest that AII may regulate plasminogen activation in the vasculature by inducing both PAI-1 and PAI-2 expression. |
| 46 | 7608643 | Whilst these correlations may represent cause and effect for plasminogen activator inhibitor, there is no evidence that changes in levels of proinsulin-like molecules influence levels of other risk factors. |
| 47 | 7792741 | In univariate analysis, PAI-1 activity correlated with serum triglycerides (rs = 0.43; p < 0.0001), insulin sensitivity (rs = -0.30; p = 0.004), and immunoreactive insulin (rs = 0.45; p < 0.0001). |
| 48 | 7792741 | However, the relationship between PAI-1 activity and plasma specific insulin (IEMA) was weaker (rs = 0.24; p = 0.019) than those with intact proinsulin (rs = 0.53; p < 0.0001) and des-31,32-proinsulin (rs = 0.54; p < 0.0001) despite the low concentrations of these proinsulin-like molecules. |
| 49 | 7792741 | In multiple regression analysis, only des-31,32-proinsulin (p = 0.001) and serum triglycerides (p = 0.013) were significant determinants of PAI-1 activity. |
| 50 | 7554780 | Serum levels of cholesterol, HDL-cholesterol, triglycerides, lipoprotein Lp(a), and the fibrinolysis factors tPA (tissue plasminogen activator) and PAI-1 activity (plasminogen activator inhibitor) were compared with sensory thresholds for vibration, electrical current perception, and pain in a population-based study comprising 239 patients with diabetes mellitus Type 1, aged 15-50 years. |
| 51 | 8722054 | A total of 135 Caucasian NIDDM subjects treated with oral therapy or diet alone were classified by the presence or absence of retinopathy, and fasting blood samples were taken for assay of PAI-1 antigen and activity, tissue plasminogen activator (t-PA), t-PA complexed with PAI-1, euglobulin clot lysis time (a measure of overall fibrinolytic activity), glucose, HbA1c, cholesterol, triglyceride, and insulin levels. |
| 52 | 8692017 | In the present study, we examined if proinsulin and insulin affect the constitutive (fasting) secretion of plasminogen activator inhibitor type 1 (PAI-1) and tissue plasminogen activator (t-PA) in young healthy women (N = 17). |
| 53 | 8692017 | We also measured the antigen concentrations of PAI-1 and t-PA during slow and fast changes in proinsulin and insulin levels induced by oral (OGTT) and intravenous (IVGTT) glucose tolerance tests. |
| 54 | 8692017 | Our findings suggest that proinsulin and insulin have no influence on the regulation of plasma levels of PAI-1 and t-PA in young healthy women, irrespective of intake of contraceptive steroids. |
| 55 | 8692017 | The clinical researchers also studied the antigen concentrations of PAI-1 and t-PA during slow and fast changes in proinsulin and insulin levels induced by oral and intravenous glucose tolerance tests. |
| 56 | 8692017 | These findings suggest that neither proinsulin nor insulin regulate plasma levels of PAI-1 and t-PA in young healthy women regardless of OC use status. |
| 57 | 8883280 | PAI-1 was positively correlated with triglycerides (r = 0.22, p = 0.024), apolipoprotein B (r = 0.21, p = 0.039) and fibrinogen (r = 0.22, p = 0.029) in cases and with BMI in both cases (r = 0.37, p = 0.0003) and controls (r = 0.23, p = 0.044). |
| 58 | 8883280 | In stepwise multiple regression analysis, only apolipoprotein B (p = 0.008) and BMI (p = 0.0014) were significant determinants of PAI-1 activity in cases. |
| 59 | 8911991 | Sulfonylureas, in contrast to insulin, seem able to inhibit the fibrinolytic system, possibly via the stimulating effect of proinsulin on the endothelial PAI-1 expression. |
| 60 | 9519730 | Hypofibrinolysis caused by increased plasminogen activator inhibitor 1 (PAI-1) has been implicated in the vasculopathy of type 2 diabetes, typified by increased insulin, glucose, and triglycerides. |
| 61 | 9519730 | However, short-term infusions of insulin have not increased PAI-1 in normal subjects. |
| 62 | 9519730 | We hypothesized that induction of increased insulin accompanied by increased glucose and triglycerides would increase PAI-1. |
| 63 | 9519730 | In contrast to results with infusion of saline alone (n = 16) and euglycemic-hyperinsulinemic clamps (n = 10, serum insulin = 89 +/- 7 microU/dl), PAI-1 in blood increased significantly 6 h after the onset of infusion (15 +/- 5 ng/ml, P < 0.05 vs. baseline = 7.4 +/- 1.1, saline 6 h = 3.4 +/- 1.1, and insulin alone 6 h = 3.7 +/- 0.8) and remained elevated for an additional 6 h (combined infusion = 13.8 +/- 3.8 ng/ml, saline = 6.7 +/- 2 ng/ml, insulin alone = 7.8 +/- 1.7 ng/ml, P = 0.06). |
| 64 | 9844142 | In smooth muscle cells and mesangial cells, the angiotensin II synthesized by ACE increases mRNA expression and the activity of PAI-1, which promotes antifibrinolysis and the accumulation of extracellular matrix. |
| 65 | 10656230 | In the 2nd group, significant reductions in markers of platelet function (FP4 and betaTG, P < 0.01), thrombin generation (FPA, F1 + 2 and D-D, P<0.01), and fibrinolysis inhibition (PAI-1 activity, PAI-1 antigen, P< 0.001) were observed. |
| 66 | 10798271 | This prothrombotic, proinflammatory state is characterised by vaso-constriction, platelet and leukocyte activation and adhesion (externalization, expression and upregulation of von Willebrand factor, platelet activating factor, P-selectin, ICAM-1, IL-8, MCP-1, TNF alpha, etc.), promotion of thrombin formation, coagulation and fibrin deposition at the vascular wall (expression of tissue factor, PAI-1, phosphatidyl serine, etc.) and, in platelet-leukocyte coaggregates, additional inflammatory interactions via attachment of platelet CD40-ligand to endothelial, monocyte and B-cell CD40. |
| 67 | 11120352 | They produce antithrombotic and thrombotic factors such as t-PA and PAI-1 and respond to TNFalpha, an important factor correlated with the inflammatory process by modifying growth characteristics by producing cytokines such as GM-CSF by expressing ICAM-1 on the surface and by producing large amounts of nitric oxide and endothelin. |
| 68 | 11126235 | Analysis of these animals demonstrated that the genetic absence of TNF signaling in obesity: (i) significantly improves insulin receptor signaling capacity and consequently insulin sensitivity; (ii) prevents brown adipose tissue atrophy and beta3-adrenoreceptor deficiency and improves thermo-adaptive responses, (iii) decreases the elevated PAI-1 and TGFbeta production; and (iv) lowers hyperlipidemia and hyperleptinemia. |
| 69 | 11230363 | These data suggest that PPARgamma activation may directly attenuate diabetic glomerular disease, possibly by inhibiting mesangial growth, which occurs early in the process of diabetic nephropathy, or by inhibiting PAI-1 expression. |
| 70 | 11423472 | Among the factors responsible for the increases of PAI-1, insulin has recently attracted attention. |
| 71 | 11423472 | By using inhibitors of the different signaling pathways evoked by insulin-receptor binding, it has been shown that the biosynthesis of PAI-1 is due to phosphatidylinositol (PI) 3-kinase activation, followed by protein kinase C and ultimately by mitogen-activated protein (MAP) kinase activation and extracellular signal-regulated kinase 2 phosphorylation. |
| 72 | 11423472 | A construct comprising four tandem repeat copies of the -93/-62 region of the PAI-1 promoter linked to CAT was transcriptionally activated in HepG2 cells by insulin. |
| 73 | 11423472 | These results outline the central role of MAP kinase activation in the regulation of PAI-1 induced by insulin. |
| 74 | 11425779 | Inhibition of ACE activity initiated in obese mice 10 weeks of age and continued for 20 weeks arrested the increase in PAI-1 activity in blood and in cardiac PAI-1 and tissue factor mRNA as well as coronary perivascular fibrosis. |
| 75 | 11852811 | Concentration of: tissue plasminogen activator antigen (t-PA:Ag), urokinase plasminogen activator antigen (u-PA:Ag), plasminogen activator inhibitor type 1 antigen (PAI-1:Ag) (ELISA), PAI-1 activity (PAI-1 act.), euglobulin lysis time (ELT) (Kowarzyk-Buluk method), fibrinogen, fibrin degradation products (FDP) (Merskey method) in blood plasma were evaluated. |
| 76 | 11916936 | In contrast to PAI-1, the association of CRP and fibrinogen with incident diabetes was significantly attenuated after adjustment for body fat (BMI or waist circumference) or insulin sensitivity (S(I)), as assessed by a frequently sampled intravenous glucose tolerance test. |
| 77 | 11991216 | These findings indicate that perindopril but not losartan decreases PAI-1 in hypertensive type 2 diabetic patients, which suggests that the PAI-1 lowering effect is unrelated with AT, receptor blockade and could rather be due to the fact that the endothelial receptors that mediate PAI-1 expression in response to angiotensin II are not type 1 receptor subtypes. |
| 78 | 11919188 | These data suggested that a member of the Forkhead/winged helix family of transcription factors mediated the effect of insulin on PAI-1 transcription. |
| 79 | 12660878 | Leptin was positively correlated with PAI-1 activity and antigen (r = 0.32, p = 0.006 and r = 0.37, p < 0.001, respectively) and negatively with t-PA activity (r = -0.27, p = 0.03). |
| 80 | 13679655 | TNF pathway and TGFb play an important role in the regulation of PAI-1 synthesis in the adipose tissue and the liver with steatosis. |
| 81 | 12830340 | The aim of this study was to compare the effects of benazepril and amlodipine in monotherapy versus in combination with plasma t-PA and PAI-1 activity in hypertensive type-2 diabetic patients. |
| 82 | 12830340 | Benazepril monotherapy significantly decreased plasma PAI-1 activity (-8.4 IU/ml, P<0.05) while it did not influence t-PA activity (+0.02 IU/ml). |
| 83 | 12830340 | Amlodipine monotherapy produced a significant increase in t-PA activity (+0.27 IU/ml, P<0.05) while it did not influence PAI-1 activity (+0.8 IU/ml). |
| 84 | 12830340 | The amlodipine/benazepril combination produced both a significant decrease in plasma PAI-1 activity (-8.7 IU, P<0.05) and a significant increase in t-PA activity (+0.26 IU/ml, P<0.05). |
| 85 | 12940867 | The aim of this study was to investigate the effect of insulin and an insulin-sensitizing agent, rosiglitazone (RSG), on the production of plasminogen-activator inhibitor-1 (PAI-1) in isolated subcutaneous abdominal adipocytes. |
| 86 | 12940867 | In contrast, insulin + RSG (10-8 m) reduced PAI-1 production relative to insulin alone (***p < 0.001), whilst RSG alone reduced PAI-1 protein secretion in a concentration-dependent manner (RSG at 10-10 m: 50.4 +/- 2.87 ng/ml downward arrow ***; RSG at 10-5 m: 30.3 +/- 2.0 ng/ml downward arrow ***; p < 0.001). |
| 87 | 12940867 | Insulin stimulated PAI-1 secretion, whilst RSG reduced both PAI-1 secretion alone and in combination with insulin. |
| 88 | 14515181 | Moreover, insulin, as we have previously shown, directly stimulates PAI-1 production with a mechanism underlying a complex signaling network which ultimately leads to ERK activation. |
| 89 | 14515181 | Interestingly, the addition of p38 inhibitor followed by insulin and Wy-14,643 resulted in a greater than additive stimulation of PAI-1 secretion acting through ERK1/2 phosphorylation. |
| 90 | 14515181 | In conclusion, Wy-14,643 induces PAI-1 gene expression, in the presence or absence of insulin, with a mechanism which is independent on PPARalpha activation and requires signaling through the ERK1/2 signaling pathway. |
| 91 | 14550286 | Adipokines such as Plasminogen activator inhibitor-1 (PAI-1), interleukin (IL)-8, and tumor necrosis factor (TNF)-alpha are elevated in patients with obesity, insulin resistance, and type 2 diabetes. |
| 92 | 12958045 | In addition to upregulation of PAI-1, downregulation of MMP-2 and MT1-MMP might play a crucial role in coronary matrix remodeling in insulin-resistant diabetes. |
| 93 | 15069077 | We previously identified an insulin response element in the promoter of plasminogen activator inhibitor 1 (PAI-1) that was activated by an unidentified member of the forkhead/winged helix (Fox) family of transcription factors. |
| 94 | 15069077 | Mutational analysis of the PAI-1 promoter revealed that oxidative stress acted at an AP-1 site at -60/52 of the promoter. |
| 95 | 15780082 | Indeed, recombinant PAI-1 directly stimulated TGF-beta message and protein via mitogen-activated protein kinase (MAPK) signal transduction in cultured mesangial cells. |
| 96 | 15780082 | Urokinase plasminogen activator (uPA) inhibited this PAI-1 action in a dose-dependent manner. |
| 97 | 15780082 | The inhibitory effect of antibody to uPA receptor (uPAR) on PAI-1-induced TGF-beta function suggested that uPAR mediated the cellular effect of PAI-1. |
| 98 | 15780082 | PAI-1 can regulate TGF-beta expression by binding to uPAR and activating the extracellular-regulated signal kinase (ERK)/MAPK pathway. |
| 99 | 15780823 | Therefore, direct inhibition of PAI-1 might not only provide a new therapeutic strategy for reducing cardiovascular risk, but may also have beneficial effects on obesity and insulin resistance. |
| 100 | 15840023 | Since both high glucose and TGF-beta1 induce cellular ROS and ROS mediate both high glucose- and TGF-beta1-induced PAI-1, ROS appear to amplify TGF-beta1 signaling in high glucose-induced PAI-1 up-regulation. |
| 101 | 15953128 | To explore the role of tissue plasminogen activator (tPA) activity and plasminogen activator inhibitor type 1 (PAI-1) in survivors of a first myocardial infarction (MI). |
| 102 | 15953128 | PAI-1 activity, fibrinogen, postload insulin and -proinsulin were significantly higher and tPA activity significantly lower in MI patients in the univariate analysis. |
| 103 | 15956119 | The induction of PAI-1 expression by hyperglycemia involves oxidative stress and protein kinase C (PKC). |
| 104 | 15956119 | Hyperglycemia stimulates Rho-kinase activity via PKC- and oxidative stress-dependent pathways, leading to increased PAI-1 gene transcription. |
| 105 | 15950223 | Our results suggested that the circadian clock component, CLOCK, is involved in the diabetes-induced circadian augmentation of PAI-1 expression in the mouse heart. |
| 106 | 15917841 | Thus, human adipose tissue from nonobese individuals releases substantial amounts of IL-6, IL-8 and IL-1 RA and the gene expression of these cytokines, like that of IL-1beta and PAI-1, is regulated by TNFalpha. |
| 107 | 16078580 | The following examinations were performed at baseline and after treatment: (1) high-resolution ultrasonography to measure the diameter changes of brachial artery in response to reactive hyperemia (endothelium-dependent) and on administration of glyceryl trinitrate (endothelium-independent); (2) high resolution ultrasonography to measure combined intima-media thickness (IMT) of common carotid arteries (CCA); (3) fasting plasma plasminogen activator inhibitor type 1 (PAI-1) activity, C reactive protein (CRP) and malonic aldehyde(MDA) concentration. |
| 108 | 16078580 | The patients had impaired endothelial dependent vasodilation (EDV), elevated plasma PAI-1 activity and increased CRP and MDA concentration at baseline. |
| 109 | 16093575 | Troglitazone improved insulin sensitivity (mean increase in whole body glucose uptake 23.1 +/- 10.5% (p = 0.047)) and normalised plasma concentrations of hsCRP, tPA and TNF-alpha, whereas it did not significantly change IL-6, leptin and PAI-1. |
| 110 | 16427606 | Low plasma levels of adiponectin (hypoadiponectinemia) and elevated circulating concentrations of plasminogen activator inhibitor (PAI)-1 are causally associated with obesity-related insulin resistance and cardiovascular disease. |
| 111 | 16427606 | Taken together, these data suggest that hypoxia and ROS decrease adiponectin production and augment PAI-1 expression in adipocytes via distinct signaling pathways. |
| 112 | 16428460 | While ATF3 failed to induce expressions of VEGF and VEGFR, it regulated those of CDK2, CDK4, p8, plasminogen activator inhibitor 1, integrin alpha1, subunit and matrix metalloprotease MMP13. |
| 113 | 16555056 | By trend analyses, group L had reduced levels of PAI-1 (p=0.002), hs-CRP (p<0.0001) and TNF-alpha (p=0.006), while no significant changes were observed in the levels of leptin or adiponectin. |
| 114 | 16555056 | In the L+I group there was a reduction in PAI-1 levels (p=0.014) and an increase in levels of leptin (p<0.001). |
| 115 | 16634839 | PAI-1 inversely correlated with the insulin sensitivity index (SI) but only in women with IIS (P<0.0001). |
| 116 | 16916991 | In the obese group, plasma adiponectin concentrations showed a strong positive association with concentrations of HDL cholesterol (P <0.0001) and negative associations with LDL cholesterol, triglycerides, high-sensitivity C-reactive protein, interleukin 6, apolipoprotein B(100), soluble E-selectin, soluble vascular cellular adhesion molecule 1, plasminogen activator inhibitor 1, leukocyte count, and liver and intramyocellular fat (all P <0.03). |
| 117 | 16968575 | RSG + MET reduced C-reactive protein (CRP; -23.9%; 95% CI: -40.4 to -2.8), plasminogen activator inhibitor-1 (PAI-1) activity (-30.1%; 95% CI: -44.5 to -11.9), PAI-1 antigen (-15.5%; 95% CI: -28.3 to -0.3) and matrix metalloproteinase-9 (MMP-9; -13.8%; 95% CI: -25.1 to -0.9), but increased tumor necrosis factor-alpha (TNF-alpha; 27.0%; 95% CI: 6.8 to 50.9). |
| 118 | 16968575 | Corresponding values for up-titrated MET were CRP -9.3% (95% CI: -36.9 to 30.2), PAI-1 activity -7.2% (95% CI: -28.2 to 20.0), PAI-1 antigen -1.5% (95% CI: -17.4 to 17.5), MMP-9 29.0% (95% CI: -1.3 to 68.6) and TNF-alpha -6.0% (95% CI: -22.0 to 13.2). |
| 119 | 17046548 | Incubation of THLE-5b cells with TNF-alpha stimulated PAI-1 production via protein kinase C-, mitogen-activated protein kinase-, protein tyrosine kinase-, and nuclear factor-kappaB-dependent pathways. |
| 120 | 17046548 | A thiazolidinedione, pioglitazone, reduced TNF-alpha-induced PAI-1 production by 32%, via protein kinase C- and nuclear factor-kappaB-dependent pathways. |
| 121 | 16741355 | Plasma adiponectin was inversely related to PAI-1 activity (r = -0.09, p = 0.03) and antigen (r = -0.202, p < 0.001). |
| 122 | 16741355 | Multiple linear regression analysis in all study subjects, in men and in normotensives documented an impact of adiponectin T94G genotype on plasma levels of adiponectin (p = 0.007, 0.003 and 0.03) and PAI-1 activity (p = 0.02, 0.03 and 0.04) and antigen (p = 0.03, 0.007 and 0.04) after adjustment for potential confounding factors. |
| 123 | 16764881 | PAI-1 did not correlate with either SBP or DBP but was related to body mass index, diabetes, and dyslipidemia. |
| 124 | 17230448 | This study shows that adipose tissue evolved into a major PAI-1 producing organ by gaining capacity during adipocyte differentiation to respond to inducers of PAI-1 transcription. |
| 125 | 17230448 | Depletion of E2F1-3 was sufficient for inducers such as insulin to potently induce PAI-1 gene expression in pre-adipocytes. |
| 126 | 17259369 | Treatment with glycated LDL increased the expression of HSF1 and Hsp-70 compared with LDL in subconfluent HCAECs or HUVECs, and that was associated with an increase of PAI-1 expression. |
| 127 | 17259369 | The transfection of HSF1 gene enhanced the expression of PAI-1 in endothelial cells. |
| 128 | 17259369 | The results suggest that HSF-1 is involved in glycated LDL-induced upregulation of PAI-1 in subconfluent vascular endothelial cells through the binding of HSF1 to PAI-1 promoter. |
| 129 | 17495595 | PAI-1 may play several roles in contributing to obesity: through indirect effects on insulin signalling, by influencing adipocyte differentiation and by regulating recruitment of inflammatory cells within adipose tissue. |
| 130 | 17452404 | Furthermore, it augmented ECM, Matrix metalloproteinase-2 (MMP), MMP-9, plasminogen activator inhibitor-1 (PAI) and tissue inhibitor of metalloproteinase-1 (TIMP) gene expression and pERK1/2 immunostaining. |
| 131 | 17728702 | Collagen IV gene expression was completely normalized by TGF-beta neutralization; however, this was associated with plasminogen activator inhibitor-1 (PAI-1) overexpression and a modest reduction in collagen protein. |
| 132 | 17728702 | Our studies suggest that prolonged exposure to HG results in PKC-delta-driven collagen accumulation by MCs mediated by PAI-1 but independent of TGF-beta. |
| 133 | 17275007 | Pretreatment with a Rho-kinase inhibitor, Y-27632 (1-10 microM), significantly blocked high glucose-induced PAI-1 expression. |
| 134 | 17275007 | NF-kappaB activity determined using the luciferase reporter gene assay was significantly enhanced by high glucose, and pretreatment with Y-27632 inhibited high glucose-induced PAI-1 expression at the basal level. |
| 135 | 17275007 | An inhibitor of NF-kappaB action, namely parthenolide (0.1 microM), BAY 11-7082 (5 microM) and SN50 (1 microM), significantly blocked high glucose-mediated PAI-1 expression to a level with low glucose (5.7 mM). |
| 136 | 17275007 | These data suggested that high glucose-induced PAI-1 expression in endothelial cells is mediated by NF-kappaB activation through the Rho/Rho-kinase pathway. |
| 137 | 18078928 | These results suggest that TNF-alpha and the local renin-angiotensin system coordinately stimulate PAI-1 production in hepatocytes. |
| 138 | 18180317 | The effect of GLP-1 on PAI-1 expression in vascular endothelial cells has not been explored. |
| 139 | 18180317 | In a spontaneously transformed human umbilical vein endothelial cell (HUVEC) line, C11-spontaneously transformed HUVEC (STH) and primary HUVEC cells, GLP-1 treatment, in the presence of a dipeptidyl peptidase IV inhibitor, attenuated induction of PAI-1 protein and mRNA expression by tumour necrosis factor-alpha (TNF-alpha). |
| 140 | 18180317 | GLP-1 also inhibited the effect of TNF-alpha on a reporter gene construct harbouring the proximal PAI-1 promoter. |
| 141 | 18180317 | In addition, GLP-1 attenuated TNF-alpha-mediated induction of Nur77 mRNA and TNF-alpha-mediated binding of nuclear proteins (NPs) to the PAI-1, Nur77, cis-acting response element nerve growth factor induced clone B response element (NBRE). |
| 142 | 18180317 | Taken together, these observations suggest that GLP-1 inhibits TNF-alpha-mediated PAI-1 induction in vascular endothelial cells, and this effect may involve Akt-mediated signalling events and the modulation of Nur77 expression and NP binding to the PAI-1 NBRE. |
| 143 | 17433639 | "In vitro" studies have demonstrated that CRP induces plasminogen activator inhibitor type 1 (PAI-1) expression, suggesting a hypofibrinolytic role for CRP. |
| 144 | 17433639 | These findings demonstrate that CRP plays an important role in the complex mechanism regulating PAI-1 antigen in 4G diabetic carriers. |
| 145 | 18596725 | ARB treatment significantly improved insulin sensitivity and markedly suppressed AT2-induced oxidative stress, PAI-1 and MCP-1 levels and NF-kappaB activation of adipocytes in culture. |
| 146 | 18597060 | OxVLDL stimulated the expression of PAI-1 from MEF of wild-type mice, but failed to increase PAI-1 expression in MEF of HSF1-knockout mice. |
| 147 | 18597060 | The results indicate that oxVLDL increased PAI-1 expression, and HSF1 mediates the transcription of PAI-1 in cultured vascular EC or fibroblasts. |
| 148 | 18566293 | Using a hyperinsulinemic clamp in young rats, we show that experimental activation of HBP, through the systemic infusion of glucosamine, induced severe insulin resistance (36% decline in peripheral insulin action; P<0.05), increased adipose tissue gene expression of fat-derived peptides (PAI-1 by 4-fold, angiotensinogen 3-fold, leptin 2-fold, resistin 4-fold, and adiponectin 4-fold; P<0.01 compared with young saline-infused), and enhanced glycosylation of transcription factors, thus mimicking a physiological and biological phenotype of aging. |
| 149 | 19100414 | We also assessed markers of endothelial cell injury-von Villebrand factor (vWF), thrombomodulin, intracellular adhesion molecule (ICAM), and CD146; markers of inflammation-high-sensitivity-reactive protein (hsCRP); other hemostatic parameters-tissue plasminogen activator (tPA) and its inhibitor (PAI-1); as well as other adipocytokines-adiponectin and resistin-using commercially available kits. |
| 150 | 19132222 | Especially a defective insulin response in the liver contributes to the development of hyperglycemia, dyslipidemia and peripheral insulin resistance and may contribute to hepatic over-expression of PAI-1 in diabetes type 2. |
| 151 | 19156184 | After Santoro II operation an adaptation of the gastric chamber size to hypercaloric diet and it removes the sources of ghrelin and aims at moderate restriction with early saciety by distention , omentectomy removes the sources of plasminogen activator inhibitor -1 (PAI-1) and resistin production, enterectomy leads more nutrients to the distal bowel and raising the levels of glucagon-like peptide -1 (GLP-1) , Peptide YY (PYY) and oxintomodulina (OXM) with desirable metabolic consequences. |
| 152 | 19337558 | The present study aimed to compare skin microvascular function, pulse wave velocity (PWV), and a variety of hemostatic markers of endothelium injury [von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1), tissue plasminogen activator (t-PA), tissue factor pathway inhibitor (TFPI), and the soluble form of thrombomodulin (s-TM)] in patients with NIDDM. 54 patients with NIDDM and 38 sex- and age-matched controls were studied. 27 diabetics had no overt micro- and/or macrovascular complications, while the remainder had either or both. |
| 153 | 18945481 | The relationship between early asymptomatic lower extremity arterial disease and blood levels of HbA1c, lipids and fibrinolysis markers (tPA-activity, tPA mass, PAI-1 activity, tPA-PAI-1 complex) was assessed. |
| 154 | 19387897 | The circadian expression of PAI-1 gene is thought to be directly regulated by the circadian clock proteins such as CLOCK and BMAL1/BMAL2 which drive the endogenous biological clock. |
| 155 | 19397838 | In response to high glucose, several of these transcription factors regulate the gene encoding the profibrotic cytokine transforming growth factor beta, as well as genes for a range of other proteins implicated in inflammation and extracellular matrix turnover, including thrombospondin 1, the chemokine CCL2, osteopontin, fibronectin, decorin, plasminogen activator inhibitor 1 and aldose reductase. |
| 156 | 19401454 | Small-interference RNA (siRNA) for p22(phox), an essential subunit of NOX, prevented oxidized LDL-induced expression of NOX2, HSF1, and PAI-1 in EC. |
| 157 | 19608644 | Using small interfering RNA to specifically deplete each of the Fox transcription factors tested, we demonstrate that only reduction of FoxO3a inhibits insulin-increased PAI-1-Luc expression and PAI-1 mRNA accumulation. |
| 158 | 19608644 | These results suggest that FoxO3a mediates insulin-increased PAI-1 gene expression. |
| 159 | 19717532 | Adjustment for smoking and levels of tissue plasminogen activator (tPA)/plasminogen activator inhibitor 1 (PAI-1) complex, von Willebrand factor and homocysteine weakened, and adjustment for high-density lipoprotein (HDL) and fibrinogen strengthened, the relationship between epilepsy and AMI. |
| 160 | 18768333 | In Type 1 diabetes, the relationship between PAI-1 and CAC was strongest for younger participants (P=.02 for PAI-1-by-age interaction) after controlling for factors related to IR. |
| 161 | 19776253 | To link insulin resistance, aging, and cardiovascular disease, we examined the expression and glycosylation pattern of PAI-1 in liver and white adipose tissue (WAT) from adult (3 mo) and insulin-resistant old (24 mo) Wistar rats. |
| 162 | 19586629 | Cilostazol also inhibited transactivating activity at the PAI-1 promoter by Smad3, leading to a suppression of PAI-1 gene transcription. |
| 163 | 19940327 | Adipose tissue produces multiple cytokines(TNF-alpha, IL-6, PAI-1, CRP, angiotensinogen, leptin, adiponectin, visfatin, apelin, resistin)which decrease insulin sensitivity and induce inflammatory processes, endothelial dysfunction,and atherosclerosis. |
| 164 | 19786738 | PAI-1 deficiency did not affect plasma glucose significantly but reduced the fractional mesangial area, fibronectin and collagen I expression in the renal cortex after 20 weeks of diabetes as well as in HG-stimulated mesangial cells along with suppression of TGF-beta1 mRNA expression. |
| 165 | 19786738 | Recombinant PAI-1-induced fibronectin and collagen I expression was abrogated by TGF-beta1 receptor inhibitor or anti-TGF-beta antibody suggesting that the effect of PAI-1 was mediated by TGF-beta1. |
| 166 | 20059881 | VCAM-1, ICAM-1, E-selectin and P-selectin were used as markers of endothelium, tissue plasminogen activator (tPA) and its inhibitor (PAI-1) as markers of fibrinolysis. |
| 167 | 19415164 | Serum concentration of CRP was significantly correlated with BMI (gamma = 0.257, P < 0.01), WC (gamma = 0.293, P < 0.01), fat mass (gamma = 0.213, P < 0.01), total adipose tissue (gamma = 0.263, P < 0.01), visceral adipose tissue (gamma = 0.296, P < 0.01), insulin (gamma = 0.189, P = 0.047), PAI-1 (gamma = 0.206, P < 0.01), leptin (gamma = 0.322, P < 0.01), mean IMT (gamma = 0.132, P = 0.042), and HOMA-IR (gamma = 0.172, P = 0.045). |
| 168 | 19875998 | BMI and waist circumference, in separate models, explained significant variation in metabolic (insulin, lipids, blood pressure (BP)) and inflammatory/procoagulation (C-reactive protein, PAI-1 activity and antigen, and fibrinogen) risk factors. |
| 169 | 20630999 | Previous studies in our laboratory demonstrated that heat shock factor-1 (HSF1) is involved in glyLDL-induced PAI-1 overproduction in vascular endothelial cells (EC). |
| 170 | 20630999 | Small interference RNA for p22(phox) prevented glyLDL-induced expression of NOX2, HSF1, and PAI-1 in EC. |
| 171 | 20630999 | Treatment with Raf-1 inhibitor blocked glyLDL-induced increase of PAI-1 mRNA in EC. |
| 172 | 20630999 | The results suggest that RAGE, NOX, and H-Ras/Raf-1 are implicated in the up-regulation of HSF1 or PAI-1 in vascular EC under diabetes-associated metabolic stress. |
| 173 | 18370641 | Insulin resistance (IR), the underlying cause of type 2 diabetes mellitus (DM), is also associated with elevated levels of inflammatory factors, such as C reactive protein (CRP), plasminogen activator inhibitor-1 (PAI-1), and fibrinogen. |
| 174 | 18484901 | The levels of plasminogen activator inhibitor 1(PAI-1), soluble P-selectin (sP-selectin), and soluble CD40 ligand (sCD40L) play an important role in the development and progression of atherosclerosis. |
| 175 | 18931023 | However, E(2) also increased cardiac levels of proteins associated with cardiovascular injury and inflammation including, AT(1)R, protein kinase C delta (PRKCD), phosphorylated PRKC, and phosphorylated extracellular signal regulated kinase (pMAPK)3/1, plasminogen activator inhibitor-1 (PAI-1), osteopontin and ED-1, a monocyte/macrophage-specific protein. |
| 176 | 20212516 | Evidence gathered in human specimens and animal models of PD have elucidated aspects of its etiology and histopathology, showing that overexpression of transforming growth factor beta1, plasminogen activator inhibitor 1, reactive oxygen species and other profibrotic factors, which are, in most cases, assumed to be induced by trauma to the tunica albuginea, leads to myofibroblast accumulation and excessive deposition of collagen. |
| 177 | 20375985 | Furthermore, visfatin induced tyrosine phosphorylation of the insulin receptor, activated downstream insulin signaling pathways such as Erk-1, Akt, and p38 MAPK, and markedly increased the levels of TGFbeta1, PAI-1, type I collagen, and MCP-1 in both renal cells. |
| 178 | 20879971 | These genes include glucokinase (GCK), HLA antigens, insulin receptor (INSR), insulin-like growth factor-2 (IGF2), HNF4A, insulin gene (INS-VNTR), plasminogen activator inhibitor 1 (PAI-1), potassium inwardly rectifying channel subfamily J, member 11 (KCNJ11), hepatocyte nuclear factor-4a (HNF4A). |
| 179 | 20843942 | Adiponectin and CRP were inversely associated with birth weight, sum of skinfolds and percent body fat, and PAI-1 with sum of skinfolds (all P<0.05) after adjustment for confounders. |
| 180 | 20962018 | Nevertheless, PAI-1 levels were elevated in both OC and PWS patients. |
| 181 | 21414238 | Increased plasma plasminogen activator inhibitor-1 (PAI-1) activity and decreased tissue plasminogen activator (tPA) activity could be considered a true component of the metabolic syndrome (MetS) associated with an increased risk of developing cardiovascular diseases (CVD) and fibrinolytic abnormalities. |
| 182 | 21414238 | The PAI-1 activity was higher in subjects with T2D with MetS (P = 9.8 × 10?¹?) and non-diabetic subjects with MetS (P = 3.0 × 10?¹?), whereas the tPA activity was lower in T2D with MetS (P = 0.003) as compare to normal subjects. |
| 183 | 21414238 | The tPA activity negatively correlated with its antigen (R² = -0.444, P = 7.7 × 10?¹³) in normal subjects and with the PAI-1 activity and antigen (R² = -0.319, P = 9.9 × 10?¹²; R² = -0.228, P = 3.4 × 10??) in diabetic subjects. |
| 184 | 21330637 | DPP-4 inhibition significantly prevented adipose tissue infiltration by CD8(+) T-cells and M1 macrophages and decreased the expression of PAI-1. |
| 185 | 15198928 | Smad proteins transduce the TGF-beta-mediated signal, and Smad-binding CAGA sequences are present in the plasminogen activator inhibitor-1 (PAI-1) promoter. |
| 186 | 15198928 | This study examined whether glycated albumin induces PAI-1 transcription in human mesangial cells (HMC) through Smad-binding sites in the PAI-1 promoter. |
| 187 | 15198928 | Transfection of phosphorothioate CAGA oligonucleotide, a CAGA antisense analog, inhibited Gly-BSA-induced PAI-1 mRNA expression. |
| 188 | 15198928 | These results indicate that Gly-BSA increases DNA binding activity of Smad3 and that it stimulates PAI-1 transcription through Smad-binding CAGA sequences in the PAI-1 promoter in HMC. |
| 189 | 15198928 | Thus progression of diabetic nephropathy may be promoted by PAI-1 upregulation mediated by the glycated albumin-induced Smad/DNA interactions. |
| 190 | 16896180 | The decreased collagen I accumulation occurred simultaneously with enhanced collagen I mRNA expression in concert with marked suppression of plasminogen inhibitor type-1 (PAI-1) mRNA and protein expression. |
| 191 | 21286681 | We investigated the association of diabetes and sepsis with various endothelial activation biomarkers of cell adhesion (E-selectin, vascular cell adhesion molecule 1 [VCAM-1] and intercellular adhesion molecule 1 [ICAM-1]), coagulation (plasminogen activator inhibitor 1 [PAI-1]) and VEGF signalling (soluble fms-like tyrosine kinase-1 [sFLT-1]). |
| 192 | 21409315 | Both elevated plasminogen inhibitor 1 (PAI-1) and increased factor VII coagulant activity (FVIIc) are potential important contributors to the increased risk of cardiovascular disease in type 2 diabetes. |
| 193 | 21526116 | PVT1 expression was significantly upregulated by glucose treatment in human mesangial cells, as were levels of FN1, COL4A1, TGFB1, and PAI-1. |
| 194 | 21526116 | Importantly, PVT1 knockdown significantly reduced mRNA and protein levels of the major ECM proteins, FN1 and COL4A1, and two key regulators of ECM proteins, TGFB1 and PAI-1. |
| 195 | 21521713 | The mechanism whereby adiponectin decreases proteinuria involves an increase in nephrin expression, and an improvement of the endothelial dysfunction due to decreases in ET-1 and PAI-1, and an increase in eNOS expression in the renal cortex. |
| 196 | 20061322 | Sclerosis and plasminogen activator inhibitor-1 (PAI-1) expression were assessed at 8 and 12 weeks, and collagen I, total collagen content and phospho-smad-2 expressions were determined at 12 weeks. |
| 197 | 20061322 | Although sulodexide may affect TGF-beta activation in radiation nephropathy, this effect appeared insufficient in this model to inhibit the expressions of PAI-1 and collagen and reduce accumulation of extracellular matrix. |
| 198 | 21298325 | It was found that insulin significantly reduced IL-6-induced gene transcription of serum amyloid 1 (SAA1), serum amyloid 2 (SAA2), haptoglobin, orosomucoid, and plasmin activator inhibitor-1 (PAI-1). |
| 199 | 20066125 | We studied 8 candidate genes: renin-angiotensin system [angiotensinogen (AGT), angiotensin II receptor type 1 (AGTR1), nitric oxide synthase 3 (NOS3)]; growth factor [hepatocyte growth factor (HGF)]; transgelin (SM22); cytokine [chemokine receptor 2 (CCR2)]; coagulation-fibrinolysis system [5,10-methylenetetrahydrofolate reductase (MTHFR)]; and plasminogen activator inhibitor 1 (PAI-1). |
| 200 | 9267149 | The activities and levels of F-VII, F-X, and PAI-1 correlated with triglycerides in serum and also with fasting insulin levels in hyperlipidemic patients with atherosclerotic vascular disease. |
| 201 | 21829729 | These remodeling indices were associated with increased expression of matrix regulatory proteins matrix metalloproteinase (MMP)-9, MMP-12, tissue inhibitors of matrix metalloproteinase (TIMP)-1, TIMP-2, and plasminogen activator inhibitor-1 (PAI-1) in db/db arteries. |
| 202 | 21624046 | Plasminogen activator inhibitor-1 (PAI-1) activity, tissue plasminogen activator (t-PA) antigen, prothrombin fragment 1+2 (F(1+2)) and von Willebrand factor (vWF) were measured in fasting blood samples from 199 STEMI patients 16.5 h (median time) after admission and 3 months later. |
| 203 | 21519232 | The aim of the study was to investigate the relationship among plasminogen activator inhibitor 1 (PAI-1), thrombin-activable fibrinolysis inhibitor (TAFI), tissue plasminogen activator (t-PA), prothrombin fragments 1+2 (F1+2), glycemic control, hypertension, sex and body mass index (BMI) in DM2 patients with normoalbuminuria and microalbuminuria. |
| 204 | 21519232 | TAFI-mediated inhibition of fibrinolysis in DM2 is regulated independently from PAI-1. |
| 205 | 21406565 | Here, we demonstrate that the serine protease inhibitor plasminogen activator inhibitor 1 (PAI-1) forms an SDS-stable complex with the PC furin, which leads to the inhibition of the intra-Golgi activity of furin. |
| 206 | 21406565 | It is known that elevated PAI-1 plasma levels are correlated with the occurrence of the metabolic syndrome and type 2 diabetes, and we show that PAI-1 reduces the furin-dependent maturation and activity of the insulin receptor and ADAM17: two proteins involved in the onset of these metabolic disorders. |
| 207 | 21406565 | In addition to demonstrating that PAI-1 is an intracellular inhibitor of furin, this study also provides arguments in favor of an active role for PAI-1 in the development of metabolic disorders. |
| 208 | 21733717 | Moreover, stimulatory (plasminogen activator inhibitor 1) and inhibitory (tissue plasminogen activator) mediators of the fibrinolytic cascade were induced by leptin and resistin, leading to a balanced plasmin activity regulation. |
| 209 | 21993838 | PAI-1 is the fast acting and specific inhibitor of tissue plasminogen activator (tPA) and urokinase (uPA), the activators of plasminogen and consequently of fibrinolysis. |
| 210 | 21993838 | These molecules include transforming growth factor ? (TGF-?), tumor necrosis factor ? (TNF-?), angiotensin II and interleukin 6 (IL-6), all of which up-regulate PAI-1 in various cell types or can be up-regulated by PAI-1. |