Probable Roles of Coagulation Cascade and Fibrinolysis System in the Development of Allergic Rhinitis

2018 ◽  
Vol 33 (2) ◽  
pp. 137-144 ◽  
Author(s):  
Seung-No Hong ◽  
Yu-Lian Zhang ◽  
Chae-Seo Rhee ◽  
Dong-Young Kim
Keyword(s):  
Allergic Rhinitis ◽  
Mouse Model ◽  
Plasminogen Activator ◽  
Ar Model ◽  
Coagulation Cascade ◽  
Tissue Type ◽  
Coagulation System ◽  
Control Group ◽  
Fibrin Deposition ◽  
Type Plasminogen Activator

Background Dysregulation of the coagulation cascade and fibrinolysis system may play an etiologic role in many diseases. Allergic diseases such as bronchial asthma, atopic dermatitis, and conjunctivitis are also associated with fibrin accumulation caused by a change in hemostasis. However, only a few studies have dealt with the relationship between allergic rhinitis (AR) and the coagulation system. Objective We investigated the difference of coagulation and fibrinolysis cascade components between an AR mouse model and a control mice. Methods BALB/c mice were sensitized and challenged with ovalbumin. Multiple parameters of coagulation cascade and fibrinolysis system such as factors II, V, VII, X, and XIII; tissue-type plasminogen activator; urokinase-type plasminogen activator (u-PA); plasminogen activator inhibitor-1 (PAI-1); and fibrin were compared between the AR model group and the control group. Results The symptom scores and eosinophil counts were higher in the AR group than in the control group ( P < .01). The mRNA expression level of u-PA ( P = .040) was significantly lower, and the expression levels of factor II ( P = .038) and factor X ( P = .036) were significantly higher, in the AR group. Immunohistochemical staining revealed that most of the fibrinolysis system and coagulation cascade components were localized to the epithelium, endothelium, and submucosal glands of the nasal mucosa. u-PA was downregulated in the AR group, whereas fibrin deposition was more prominent in the AR group than in the control group. Conclusion In AR, particular components of the coagulation cascade were increased and fibrinolysis system was decreased compared to normal control. This difference may be associated with the fibrin deposition in the mucosa of AR mouse model.

Binding of 131I-Labeled Tissue-Type Plasminogen Activator on De-Endothelialized Lesions in Rabbits

1987 ◽  
Vol 26 (05) ◽  
pp. 224-228 ◽  
Author(s):  
Y. Isaka ◽  
H. Etani ◽  
K. Kimura ◽  
S. Yoneda ◽  
T. Kamada ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Abdominal Aorta ◽  
Half Life ◽  
Balloon Catheter ◽  
Biochemical Properties ◽  
Tissue Type ◽  
Fibrin Deposition ◽  
Tissue Type Plasminogen Activator ◽  
High Affinity ◽  
Type Plasminogen Activator

Tissue-type plasminogen activator (t-PA) which has a high affinity for fibrin in the clot, was labeled with 131I by the iodogen method, and its binding to de-endothelialized lesions in the rabbit was measured to assess the detectability of thrombi. The de-endothelialized lesion was induced in the abdominal aorta with a Fogarty 4F balloon catheter. Two hours after the de-endothelialization, 131I-labeled t-PA (125 ± 46 μCi) was injected intravenously. The initial half-life of the agent in blood (n = 12) was 2.9 ± 0.4 min. The degree of binding of 131I-labeled t-PA to the de-endothelialized lesion was evaluated at 15 min (n = 6) or at 30 min (n = 6) after injection of the agent. In spite of the retention of the biochemical properties of 131I-labeled t-PA and the presence of fibrin deposition at the de-endothelialized lesion, the binding of t-PA to the lesion was not sufficiently strong. Lesion-to-control ratios (cpm/g/cpm/g) were 1.65 ± 0.40 (at 15 min) and 1.39 ± 1.31 (at 30 min), and lesion-to-blood ratios were 1.39 ± 0.32 (at 15 min) and 1.36 ± 0.23 (at 30 min). These results suggest that radiolabeled t-PA may be inappropriate as a radiopharmaceutical for the scintigraphic detection of a pre-existing thrombotic lesion.

Deep Vein Thrombosis and Fibrinolysis

1991 ◽  
Vol 66 (04) ◽  
pp. 426-429 ◽  
Author(s):  
Marcel Levi ◽  
Anthonie W A Lensing ◽  
Harry R Büller ◽  
Paolo Prandoni ◽  
Gerard Dooijewaard ◽  
...  
Keyword(s):  
Deep Vein Thrombosis ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Controlled Study ◽  
First Episode ◽  
Control Group ◽  
Vein Thrombosis ◽  
Type Plasminogen Activator ◽  
Deep Vein

SummaryIn the present study 57 consecutive patients with a first episode of venographically proven deep vein thrombosis were investigated to evaluate the release of tissue-type plasminogen activator (t-PA) and of urokinase-type plasminogen activator (u-PA) in response to DDAVP stimulation as well as the resting plasminogen activator inhibitor (PAI) concentration, comparing this to the results obtained in 66 similar patients with a clinical suspicion of thrombosis but with a normal venogram. All assays were performed without knowledge of the patient's status.Four patients in the deep vein thrombosis-group (7%) had an absent u-PA antigen response upon DDAVP infusion, while a normal response was observed in all control subjects. Patients and controls showed similar increases in t-PA antigen level upon DDAVP. High resting PAI antigen levels were encountered in 5 patients in the deep vein thrombosis-group (9%) and in 6 subjects in the control group (9%).The results from this controlled study indicate that a defective release of u-PA may occur in patients with deep vein thrombosis and may have pathogenetic significance. Furthermore it is concluded that elevation of PAI levels cannot be considered as a specific risk factor for venous thrombosis.

The Changes of Tissue-Type Plasminogen Activator and Matrix Metalloproteinases in Neonatal Mice with Hypoxic-Ischemic Encephalopathy

2012 ◽  
Vol 195-196 ◽  
pp. 447-451
Author(s):  
Jian Wen Xu ◽  
Wei Wang ◽  
Xiao Zhen Zhao ◽  
Geng Zhang ◽  
Juan Bing Wei
Keyword(s):  
Matrix Metalloproteinases ◽  
Basement Membrane ◽  
Plasminogen Activator ◽  
Hypoxic Ischemic Encephalopathy ◽  
Tissue Type ◽  
Control Group ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Hypoxia Ischemia ◽  
Ischemic Encephalopathy

Fetal distress and neonatal asphyxia are key factors which result in neonatal hypoxic-ischemic encephalopathy (HIE). There is growing evidence that tissue-type plasminogen activator (TPA) and matrix metalloproteinases (MMPs) may be involved in extracellular matrix (ECM) degradation in the central nervous system. In this study, the transmission electron microscope was used to observe the growth and development characteristics of the blood-brain barrier (BBB), follow by the activity of TPA and the expression of MMPs in HIE model were detected. The asphyxia in female mice within the last day of gestation was produced by a delayed cesarean section. The experiment was designed for 1 control group and 2 asphyctic groups (15min and 30min), then the activities of TPA and expression of MMPs were detected separately. The results showed that the BBB was not fully developed in newborns, their brain microvascular endothelial cells were not surrounded with intact basement membrane and only had discontinuous basement membrane-like materials of varying thickness. The activity of TPA and the expression of MMPs of brain increased after hypoxia-ischemia in vivo. Based on these findings we concluded that the basement membrane at the BBB was a weak link in the brain, TPA and MMPs could degrade components of the ECM. So these enzymes increased after hypoxia-ischemia might be able to attack the basement membrane of microvessels, then open the BBB and induce the cerebral edema.

A global assay of haemostasis which uses recombinant tissue factor and tissue-type plasminogen activator to measure the rate of fibrin formation and fibrin degradation in plasma

2007 ◽  
Vol 98 (10) ◽  
pp. 871-882 ◽  
Author(s):  
Kun Zhu ◽  
Mika Skeppholm ◽  
Jenny Vedin ◽  
Jan Svensson ◽  
Nils Egberg ◽  
...  
Keyword(s):  
Tissue Factor ◽  
Plasminogen Activator ◽  
Coagulation Cascade ◽  
Tissue Type ◽  
Thrombin Inhibitor ◽  
Tissue Type Plasminogen Activator ◽  
Fibrin Formation ◽  
Minimal Dose ◽  
Type Plasminogen Activator ◽  
Pai 1

SummaryThe global assay of Overall Haemostasis Potential we previously described has been refined. The coagulation cascade in plateletpoor plasma is triggered by adding a minimal dose of recombinant tissue factor together with purified phospholipids and calcium; fibrinolysis is initiated by adding recombinant tissue type-plasminogen activator in a concentration similar to what can be obtained during thrombolysis. Numerical differentials of optical densities reflecting rates of fibrin formation and degradation are calculated by a new software, and the Coagulation Profile (Cp) and the Fibrinolysis Profile (Fp) are determined. The combined effect of these counteractive systems is expressed as a ratio of Cp to Fp, called the Overall Haemostasis Index. Commercially available coagulant-deficient patient plasma samples and plasma with various amounts of added PAI-1 are examined; changes of fibrin turbidity demonstrate that this assay can determine Cp and Fp in a physiologically relevant way. Increased Cp and decreased Fp in prothrombotic patients, as well as expected effects of heparin or a thrombin inhibitor on Cp and Fp, suggest that our method can detect hypercoagulability and assist in monitoring antithrombotic treatment. Ongoing studies will show whether this simple assay can be of value in clinical routine.

Stanozolol-Induced Changes in Fibrinolysis and Coagulation in Healthy Adults

1984 ◽  
Vol 51 (02) ◽  
pp. 157-164 ◽  
Author(s):  
C Kluft ◽  
F E Preston ◽  
R G Malia ◽  
R M Bertina ◽  
G Wijngaards ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Protein C ◽  
Plasma Lipids ◽  
Therapeutic Potential ◽  
Healthy Adults ◽  
Tissue Type ◽  
Coagulation System ◽  
Tissue Type Plasminogen Activator ◽  
Plasminogen Activator Activity ◽  
Type Plasminogen Activator

SummaryThe effects of orally-administered stanozolol, 5 mg b. d. on fibrinolysis, coagulation and on various haematological and biochemical parameters have been studied in 16 healthy adults, 8 males and 8 females. Statistically significant enhancement of extrinsic (tissue-type) plasminogen activator activity was detected in all subjects studied. This was associated with significant increases in plasma plasminogen and a concomitant reduction in histidine-rich glycoprotein. There were no changes in plasma urokinase activity. Changes in the coagulation system included significant reduction in plasma fibrinogen and elevation of protein C and anti thrombin III. Changes in plasma lipids included significant reduction of HDL cholesterol associated with an increase in LDL triglycerides. No change occurred in total cholesterol. There were no major differences between the sexes, nor were there serious side effects.The effects of stanozolol on extrinsic (tissue-type) plasminogen activator activity, “free” plasminogen, protein C and antithrombin III, argue strongly in favour of its therapeutic potential.

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