Immunohistochemical expression of plasminogen activator inhibitor-1 in subcutaneous versus omental adipose tissue in patients after elective abdominal surgery

Plasminogen activator inhibitor-1 (PAI-1) is a biomarker of thrombosis. Adipose and vascular tissues are among the major sources of PAI-1 production. Previous studies indicated that fat deposits mediate increased cardiovascular risk among obese individuals. We investigated the immunohistochemical (IHC) expression of PAI-1 in adipose and vascular tissues from the omentum and the subcutaneous tissue. The pathology samples were selected from 37 random patients who underwent elective abdominal surgery between 2008-2009. PAI-1 expression was semi-quantitatively scored and compared between the groups. Significant differences were noted in the IHC expression of PAI-1 between the omental and the subcutaneous adipose tissues (1.1 ± 0.8 versus 0.8 ± 0.6, respectively (p=0.05)). Adipose tissue displayed higher IHC expression of PAI-1 compared to vascular wall tissue in both omentum and subcutaneous sections (1.1 ± 0.8 versus 0.5 ± 0.9 (p=0.004), and 0.8 ± 0.6 versus 0.4 ± 0.6 (p=0.003), respectively). In conclusion, our study compared PAI-1 expression in the omentum versus the subcutaneous tissue and adipose versus vascular tissues. IHC expression of PAI-1 level was significantly higher in the omental adipose tissue compared to the subcutaneous adipose tissue. Adipose tissue displayed significantly higher PAI-1 expression than vascular tissue. The study elucidates the biological differences of adipose and vascular tissue from subcutaneous versus omental sections.

Urokinase-type plasminogen activator receptor in IgA nephropathy

No abstract available.

Urokinase, urokinase receptor, and plasminogen activator inhibitor-1 expression on podocytes in immunoglobulin A glomerulonephritis

BACKGROUND/AIMS: The purpose of this study was to investigate the expression of urokinase-type plasminogen activator (uPA), uPA receptor (uPAR), and plasminogen activator inhibitor (PAI)-1 on podocytes in immunoglobulin A (IgA) glomerulonephritis (GN). METHODS: Renal biopsy specimens from 52 IgA GN patients were deparaffinized and subjected to immunohistochemical staining for uPA, PAI-1, and uPAR. The biopsies were classified into three groups according to the expression of uPA and uPAR on podocytes: uPA, uPAR, and a negative group. The prevalences of the variables of the Oxford classification for IgA GN were compared among the groups. RESULTS: On podocytes, uPA was positive in 11 cases and uPAR was positive in 38 cases; by contrast, PAI-1 was negative in all cases. Expression of both uPA and uPAR on podocytes was less frequently accompanied by tubulointerstitial fibrosis. CONCLUSIONS: Our results suggest a possible protective effect of podocyte uPA/uPAR expression against interstitial fibrosis.

plasminogen activator inhibitor-1 [PAI-1] gene locus 4g/5g polymorphism and PAI-1 plasma levels in Egyptian patients with myocardial infarction

Activation of inflammation and coagulation are closely related and mutually interdependent in myocardial infarction [MI]. The acute-phase protein, plasminogen activator inhibitor-1 [PAI-1], is a key element in the inhibition of fibrinolysis. Elevated levels of PAI-1 have been related to MI. There are controversial data regarding the impact of 4G/5G polymorphism of the PAI-1 gene in the pathogenesis of MI. Patients with MI exhibited significantly higher plasma PAI-1 levels than controls. Significant changes in PAI-1 levels were found in homozygous PAI-1 4G/4G carriers compared with other 4G/5G genotype carriers in patients with MI. The allelic frequency of 4G among the patients was 83.3%; that of 5G was 16.7%. In the control group, the allelic frequencies of 4G and 5G were 62.0% and 38.0% respectively. The difference in genotype distribution between the two groups was significant. There were significant associations between MI and the 4G allele, hypertension, smoking, and family history of coronary heart disease. Our findings suggest that the 4G allele of the PAI-1 promoter polymorphism is an independent risk factor for MI. The emerging evidence that circulating levels of PAI-1 relate to genotype at a common polymorphism in the promoter of the PAI-1 gene has opened the possibility of using PAI-1 genotype as a surrogate measure of pre-morbid PAI-1 levels to tease apart the cause and effect limbs of the PAI-1-coronary disease relationship. The detection of this allele along with other risk factors may therefore be useful in primary prevention

Tissue plasminogen activator and plasminogen activator inhibitor-1 in human choledochal bile

Fibrinolytic properties have been detected in animal and human gallbladder (GB) bile. Plasminogen activator inhibitor-1 (PAI-1) has been reported in greater concentration in GB stone bile and may be a nucleating factor in the pathogenesis of GB stone formation. It is unknown whether or not human choledochal bile has similar properties, which could have a role in choledocholithiasis. The aims of this study were to determine the presence of fibrinolytic properties of human choledochal bile and to compare those properties among normal, acalculous, and calculous-infected choledochal bile. Tissue plasminogen activator (t-PA) and PAI-1 of choledochal bile were measured by enzyme linked immunosorbent assay in patients with cholangitis due to acalculous bile duct obstructions (n = 9), choledocholithiasis with cholangitis (n = 20), and normal bile (n = 7). The t-PA concentration of choledochal bile was no different among the three groups (acalculous-infected bile, median 4.61 ng/ml, and calculous-infected bile, 4.61 ng/ml, versus normal bile, 7.33 ng/ml). PAI-1 was detected in choledochal bile in significantly greater concentrations in patients with acalculous cholangitis due to bile duct obstructions and choledocholithiasis with cholangitis (acalculous-infected bile, median 0.36 ng/ml, and calculous-infected bile, 0.1 ng/ml, versus normal bile, 0.02 ng/ml, p < 0.05), but the bile concentration of PAI-1 was no different between the acalculous and calculous-infected choledochal bile. Human choledochal bile possesses t-PA and PAI-1. PAI-1 was present in greater concentrations in both acalculous and calculous-infected choledochal bile. Increased levels of PAI-1 may be an epiphenomenon of cholangitis rather than a factor in the pathogenesis of choledocholithiasis.

Relationship between tissue plasminogen activator, plasminogen activator inhibitor and CT image in chronic subdural hematoma

The present study was performed to investigate the relationship between the concentrations of tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) and the CT images in 23 cases of chronic subdural hematomas (SDHs). The concentrations of t-PA and PAI-1 were quantified by enzyme-linked immunosorbent assay (ELISA). Chronic SDHs were divided into five groups according to their appearance on computed tomography: high-density (n = 4), isodensity (n = 8), low-density (n = 5), mixed-density (n = 3), layering (n = 3) types. The volume of hematoma was measured with an image analyzing software program. The concentrations of t-PA were higher in layering (41.2 +/- 0.3 ng/ml, mean +/- standard error of the mean) and high-density (40.0 +/- 1.1 ng/ml) types compared to those of low-density (23.3 +/- 4.1 ng/ml) and iso-density (25.1 +/- 3.7 ng/ml) types. The concentrations of PAI-1 were lower in layering (95.9 +/- 1.0 ng/ml) and high-density (103.4 +/- 34.5 ng/ml) types compared to that of low-density (192.5 +/- 2.6 ng/ml) type. So the ratio between t-PA and PAI-1 (t-PA/PAI) was greater in layering and high-density types. The volume of hematoma was larger in mixed-density and layering types but statistically insignificant. These results presumably suggest that the ratio between t-PA and PAI concentration may contribute to the pathogenesis of the chronic SDH.

Plasminogen activator inhibitor-1 in central and peripheral obesity

In the present study, one component of fibrinolytic system [PAI-1] was examined in obese middle aged females with a high and low waist hip ratio [WHR] in comparison to lean age and sex matched group. The study comprised 15 obese female subjects with a high WHR, 15 obese female subjects with a low WHR and 10 non obese females. PAI-1 was significantly elevated in the obese women with a high WHR compared with the obese women with a low WHR or with lean women. In addition, obese women with a high WHR exhibited a greater metabolic risk profile [elevated glucose, cholesterol and triglyceride levels]. When all subjects were pooled for analysis, PAI-1 levels correlated positively with glucose and cholesterol levels. In conclusion, the data showed that a high WHR in obese females is associated with an impaired fibrinolytic activity due to increased plasma PAI-1 level. In addition, obese females with high WHR are liable to a high metabolic risk profiles