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Plasminogen Activator System (plasminogen + activator_system)
Selected AbstractsThe Effects of Cyclooxygenase2,ProstaglandinE2 Pathway on Helicobacter pylori -Induced Urokinase-Type Plasminogen Activator System in the Gastric Cancer CellsHELICOBACTER, Issue 3 2008Junichi Iwamoto Abstract Background:, Urokinase-type plasminogen activator (uPA) and its receptor (uPAR) play an important role in the destruction of the extracellular matrix and basement membrane. The induction of uPA and uPAR in the gastric cancer cells with H. pylori has been demonstrated previously. The involvement of COX-2-PGE2 pathway in the uPA system (uPA and uPAR) expression is unclear. Methods:, Gastric cancer cells (MKN45) were co-cultured with H. pylori standard strain (NCTC11637). The specific inductions of uPA and uPAR mRNA were examined by reverse transcription-polymerase chain reaction amplification. The secreted uPA antigen was measured by ELISA. To evaluate the involvement of COX-2 and PGE2 pathway in H. pylori -induced uPA and uPAR expressions, we examined the effects of COX-2 inhibitor and PGE2 receptor antagonist on H. pylori -induced uPA and uPAR expression in the gastric cancer cells. Results:, The expressions of both uPA and uPAR mRNAs in the gastric cancer cells increased obviously (12-fold and 3-fold, respectively) with H. pylori stimulation. The amount of uPA antigen into the culture medium increased dramatically with H. pylori stimulation. The COX-2 expression level in the gastric cancer cells increased remarkably with H. pylori stimulation. H. pylori -induced uPA and uPAR expression levels were suppressed with COX2 inhibitor treatment. The amount of PGE2 antigen into the culture medium increased dramatically 24 hours after H. pylori stimulation. The gastric cancer cells expressed EP2 and EP4 subtypes. EP2 receptor antagonist suppressed the H. pylori -induced uPA and uPAR expressions in the gastric cancer cells. Conclusions:, Our results indicated that COX2-PGE2 pathway may be involved in H. pylori- associated uPA and uPAR induction, and that COX-2 inhibitor or EP2 receptor antagonist may inhibit angiogenesis and tumor invasion via suppression of the uPA system. [source] Comparison of two in vivo models for prostate cancer: Orthotopic and intratesticular inoculation of LNCaP or PC-3 cellsINTERNATIONAL JOURNAL OF UROLOGY, Issue 12 2004KIYOSHI KOSHIDA Abstract, Background:, The critical events in the clinical course of prostate cancer are the occurrence of metastasis and the induction of the hormone-refractory status of the disease. In order to investigate the factors responsible for these events, we need appropriate in vivo models. Materials and methods:, Orthotopic and intratesticular models were created by the injection of LNCaP cells or PC-3 cells into the prostate or testis of severe combined immunodeficient mice. Results:, LNCaP cells in the intratesticular model showed a higher incidence of tumor formation and lymph node metastasis when compared with those in the orthotopic model, while PC-3 cells were highly tumorigenic and metastastic in both models. A high concentration of androgens might play a role in tumor aggressiveness of LNCaP cells, given that enhanced mRNA expressions of integrin ,V and vascular endothelial growth factor was induced by dehydrotestosterone administration in vitro. The high expression of metastasis-related genes, including the urokinase plasminogen activator system, metalloproteinases and vascular endothelial growth factor-C, might be attributed to the high metastatic potential in both models. Interestingly, testicular xenografts of LNCaP cells were able to survive on the subcutis back of castrated male mice as well female mice. Conclusions:, Intratesticular models of prostate cancer appear to be suitable for studying the mechanisms of metastasis and for evaluating various treatment strategies. [source] Post-transcriptional regulation of plasminogen activator inhibitor-1 by intracellular iron in cultured human lung fibroblasts,interaction of an 81-kDa nuclear protein with the 3,-UTRJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 5 2005K. S. RADHA Summary., The proteinase inhibitor, type-1 plasminogen activator inhibitor (PAI-1), is a major regulator of the plasminogen activator system involved in plasmin formation and fibrinolysis. The present study explores the effects of intracellular iron on the expression of PAI-1 and associated cell-surface plasmin activity in human lung fibroblasts; and reports the presence of a novel iron-responsive protein. ELISA revealed a dose-dependent increase in PAI-1 antigen levels expressed in the conditioned medium of cells treated with deferoxamine, in the three cell lines studied. A concomitant increase in mRNA levels was also observed by Northern analyses. Presaturation with ferric citrate quenched the effect of deferoxamine. Experiments with transcription and translation inhibitors on TIG 3-20 cells demonstrated that intracellular iron modulated PAI-1 expression at the post-transcriptional level with the requirement of de-novo protein synthesis. Electrophoretic mobility shift assay and UV crosslinking assays revealed the presence of an ,,81-kDa nuclear protein that interacted with the 3,-UTR of PAI-1 mRNA in an iron-sensitive manner. Finally, we demonstrated that the increased PAI-1 is functional in suppressing cell-surface plasmin activity, a process that can affect wound healing and tissue remodeling. [source] Gingival status, crevicular fluid tissue-type plasminogen activator, plasminogen activator inhibitor-2 levels in pregnancy versus post-partumAUSTRALIAN DENTAL JOURNAL, Issue 3 2010N Buduneli Abstract Background:, This study was conducted to evaluate a possible link between periodontal status of pregnant women and the plasminogen activator system in gingival crevicular fluid (GCF). Methods:, GCF samples were obtained from four interproximal sites of anterior teeth in 43 women during the second trimester and also after delivery. Full mouth dental plaque, bleeding on probing (BOP) and probing depth (PD) values were recorded at six sites/tooth in each subject. GCF levels of tissue type plasminogen activator (t-PA) and its inhibitor, plasminogen activator-inhibitor-2 (PAI-2) were determined by ELISA. Data comparisons between pregnancy and post-partum were made by Wilcoxon signed rank test. Results:, The number of pockets with a PD >4 mm and total volume of GCF sampled were reduced significantly after delivery (p = 0.000 and p = 0.013, respectively). No significant differences were detected in GCF concentrations of t-PA or PAI-2 between pregnancy and post-partum. Conclusions:, Our results suggest that GCF t-PA and PAI-2 concentrations are not affected by pregnancy. Reductions in PD values and GCF volume following delivery indicate a resolution of oedema in gingival tissues, possibly related to hormonal changes due to the ending of pregnancy. [source] | ||||||||||