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Abstract: The aim of this study was to analyze and compare the immunohistochemical expression of plasminogen activator system (PAS) proteins (uPA, uPAR, and PAI-1) in ameloblastomas (AMBs), odontogenic keratocysts (OKCs), and dental follicles (DFs) representing normal odontogenic tissue, as well as to investigate possible correlations between these proteins. Twenty AMBs, 20 OKCs, and 10 DFs were selected for immunohistochemical analysis. In each case, the immunoexpression of uPA, uPAR, and PAI-1 was evaluated semiquantitatively based on the percentage of positivity in odontogenic epithelial and connective tissue cells. The epithelial immunoexpression of uPA was significantly lower in AMBs when compared to OKCs (p = 0.001) and DFs (p = 0.029). Significantly higher epithelial immunostaining for uPAR was observed in AMBs when compared to OKCs (p < 0.001). There were no significant differences in the epithelial immunoexpression of PAI-1 between AMBs and OKCs (p = 1.000). The correlations found for the expression of the studied proteins were not statistically significant (p > 0.05). However, the epithelial and connective tissue expressions of uPAR have a strong positive and statistically significant correlation in AMBs. The present results suggest that uPA is involved in the pathogenesis of OKCs and that uPAR may participate in tumorigenesis in AMBs. The high percentage of PAI-1-positive cells suggests a possible role for this protein in the development of AMBs and OKCs. Furthermore, the studied proteins do not seem to act synergistically in AMBs, OKCs, and DFs.
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Recurrent pregnancy loss (RPL) is a common complication of pregnancy, which affects 2%fertile women. A recent research has found that high level of thrombin-activatable fibrinolysis inhibitor (TAFI) can reduce the occurrence risk of early RPL. TAFI is one kind of carboxypeptidase, which can be activated as TAFIa. TAFIa can make the fibrinolysin lose its working site, which can interact with the fibrin to play a role in the regulation of fibrinolysis and the inhibition of throm?bus formation. The damage of fibrinolytic system is one of the risk factors for the occurrence of RPL in pregnant women, which has become one of the hotspots in the medical profession. In this paper, recent literature on TAFI and its relationship with recurrent pregnancy loss has been reviewed, hoping for new ways and clues in clinical treatment and prevention of RPL.
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Objective To evaluate the relationship of thrombin activated fibrinolysis inhibitor (TAFI) in plasma with changes of coagulant and fibrinolytic function in type 2 diabetes.Methods The plasma level of TAFI was measured by ELISA, fibrinogen was analyzed with Clauss assay and plasminogen was detected by chromogenic assay.Results The plasma levels of TAFI, Fib and the activity of PLG were significantly increased in type 2 diabetes with (P
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Diabetic nephropathy is characterized by an expansion of the glomerular mesangium, caused by mesangial cell proliferation and an excessive accumulation of extracellar matrix (ECM) proteins, which eventually leading to glomerulosclerosis. TGF-beta1 was found to play an important role in the accumulation of ECM in the kidney. In this study, TGF-beta1 RNA interference was used as an effective therapeutic strategy. The inhibitory effect of TGF-beta1 small interfering RNAs (siRNAs) on the high glucose-induced overexpression of TGF-beta1 in rat mesangial ceys (RMCs). A high levels of glucose induces TGF-beta1 mRNA and protein, and TGF-beta1 siRNAs reduce the ability of high glucose to stimulate their expression. We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. In conclusion, the present study demonstrates that TGF-beta1 siRNAs effectively inhibits TGF-beta1 mRNA and protein expression in RMCs. These suggest that TGF-beta1 siRNAs through RNAi may be a useful tool for developing new therapeutic applications for the treatment of diabetic nephropathy.
Subject(s)
Rats , Male , Animals , Transforming Growth Factor beta1/metabolism , Rats, Sprague-Dawley , RNA, Small Interfering/metabolism , Microscopy, Fluorescence , Mesangial Cells/metabolism , Glucose/metabolism , Glomerular Mesangium/metabolism , Gene Expression Regulation , Diabetic Nephropathies/pathology , Collagen Type I/metabolism , Cells, Cultured , Cell ProliferationABSTRACT
Objective To study the effects and clinical significance of plasma thromboxane B2(TXB2), platelet alpha granule membrance protein-140(GMP-140), 6-Keto-PGF1?(6-K-PGF1?), endothelins(ET), tissue type plasminogen activator(tPA) and plaminogen activator inhibitor-1(PAI-1) in patients with cerebral arteriosclerisis and cerebral thrombosis. Methods Plasma TXB2 ,GMP-140,6-K-PGFla and ET levels were determined by ra-dioimmuno-assay. Plasma tPA and PA1 were determined by the chromogenic peptide substrate method in controls and in patients with cerebral arteriosclerisis and cerebral thrombosis. Results The levels of plasma TXB2 and GMP-140 were significantly higher in patients with cerebral arteriosclerisis and cerebral thrombosis than in the control group(P0.05) .The levels of tPA and tPA/PAI were significantly lower in patients with cerebral arteriosclerisis and cerebral thrombosis than in controls. Although the PAI level increased in patients with cerebral arteriosclerisis and cerebral thrombosis,no difference was found in statistics. Conclusions Activation of platelets, injury of endothelial cell and decreased activity of fibrinolysis in patients with cerebrovascular disease may be involved in the development of these diseases. Appropriate treatment should be adopted on the above abnormality.
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Objective To investigate the role of antisense RNA of plasminogen activator inhibitor 1 (PAI 1) in regulating the expression of PAI 1 and vascular endothelial growth factor (VEGF) in aorta endothelial cells (EC) cultured in vitro. Methods The second extron of PAI 1 was amplified by polymerase chain reaction(PCR) and the product was inserted into eukaryotic cell expression vector pcDNA3.1(-) to construct PAI 1 antisence RNA recombinant plasmid. The recombinant plasmid was transfected into EC and the PAI 1 expression was detected by immunohistochemistry, Westernblot and ELISA. The effects of PAI 1 variation on VEGF were examined by immunofluorescence method. Results PAI 1 antigen was the lowest (0 017 ng/ml) in cells and the immunofluorescence representing the expression of VEGF in the cytoplasm showed the weakest at the third day after transfection. At the fifth day, PAI 1 antigen increased to 0 093 ng/ml with VEGF expression increased correspondingly. At the seventh day, PAI 1 antigen(0 143 ng/ml) and VEGF increased closed to normal level. Conclusions PAI 1 antisense RNA blocked the translation of PAI 1 proteins effectively and inhibited the expression of VEGF in aorta endothelial cells.
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Objective To investigate the relationship between plasminogen activator inhibitor(PAI) activity and coronary artery disease(CAD) in elderly patients. Methods Plasma samples from 93 patients with CAD were analyzed for the PAI activity, plasminogen activator(t-PA) activity, serum levels of cholesterol and triglyceride. The values of these parameters were compared between the CAD and the control groups. Results Higher plasma PAI activity 〔(810?360) AU/L vs. (640?300) AU/L,P
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砄bjective:To investigate the expression of plasminogen activator inhibitor 1(PAI 1) in oral and maxillofacial tumors and the relationship between PAI 1 and pathological parameters.Methods:Chromogenic substrate assay was used to determine PAI 1 level in tumor tissues and ELISA was used to detect the concentration of PAI 1 in tissue extracts in 30 cases of malignant tumors and 10 of benign tumors in oral and maxillofacial area.Results:Higher level and concentration of PAI 1 were found in malignant tumors than in tumor adjacent tissues or benign tumors ( P
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AIM: To investigate the expression of peroxisome proliferator-activated receptors (PPARs) in human endothelial cells, and their effects on plasminogen activator inhibitor-1 transcription. METHODS: The expression of three types of PPARs in mRNA level were detected in human umbilical vein endothelial cells(HUVECs) by using RT-PCR. Cultured endothelial cells line-ECV304 were transfected with PAI-1 promoter controlling CAT reporter gene and co-transfected with varying doses (250, 500, 1 000 ng) of expression vectors PPAR? or PPAR?.The transcripton activity of PAI-1 promoter were detected with ELISA. RESULTS: There were all three types of PPARs mRNA expression in HUVECs, while the expression of PPAR? was less than that of PPAR?( P