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1

Natriuretic peptides reduce plasminogen activator inhibitor-1 expression in human endothelial cells

100%
Pawlowska Z., Jerczynska H., Szemraj J., Baranska P., Swiatkowska M., Cierniewski C. S.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
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nr 4
Plasma concentrations of natriuretic peptides increase in some pathological conditions, but very little is known about the effect of these vasodilator peptides on the regulation of the blood coagulation system. The fundamental role in the regulation of fibrinolysis is played by plasminogen activator inhibitor type 1 (PAI-1). Recent studies demonstrate that natriuretic peptides can modulate PAI-1 expression in bovine aortic smooth muscle cells and rat aortic endothelial cells. In this report, we tested the effect of natriuretic peptides on PAI-1 expression in the human endothelial cell line (EA.hy 926). For this purpose, we treated the cell cultures with ANP, BNP and CNP, and modulation of PAI-1 synthesis was evaluated. We compared the effect of natriuretic peptides on synthesis and release of PAI-1 in unstimulated cells, and after activation with tumour necrosis factor α (TNFα). Natriuretic peptides abolished TNFα-induced upregulation of PAI-1 expression at both the PAI-1 mRNA and the antigen levels. The inhibitory efficiency was higher in the case of CNP when compared to that produced by ANP and BNP, particularly when TNFα-stimulated cells were used. We observed an inhibition of stimulatory effect of TNFα on PAI-1 expression also at the level of the PAI-1 promoter in cells transfected with a PAI-1 promoter fragment (+71 to -800) [1], The PAI-1 promoter activity was markedly inhibited by C-type natriuretic peptide, already at a very low (0.001 µM) concentration of the peptide.
2

Reactive oxygen species upregulate expression of PAI-1 in endothelial cells

100%
Swiatkowska M., Szemraj J., Al-Nedawi K. N. I., Pawlowska Z.
Cellular and Molecular Biology Letters
|
2002
|
tom 07
|
nr 4
Second messengers involved in the signal transduction pathway leading to induction of the plasminogen activator inhibitor (PAI-1) have not yet been well characterized. This study focuses on the mechanisms of regulation of PAI-1 expression by reactive oxygen species (ROS) in human endothelial cells. Inhibition of the tumor necrosis factor α (TNFα)-induced expression of PAI-1 by antioxidant N-acetyl-L-cysteine (NAC) indicated redox-sensitive mechanisms involved in the signalling pathway. Because TNFα induces PAI-1 production in endothelial cells, and NAC attenuated this response, we attempted to investigate the possible involvement of ROS in the activation of PAI-1 by TNFα. Upregulation of PAI-1 expression in endothelial cells by the stimulation with TNFα (50ng/ml) or H2O2 (10-200µM), observed by measurement of the antigen and mRNA levels, was reversed in the presence of NAC (20mM). The stimulatory effect of ROS was detected also at the level of the PAI-1 promoter in endothelial cells transfected with plasmid p800 LUC containing a PAI-1 promoter fragment (+71 to -800). The PAI-1 promoter activity was increased in the presence of ROS, and was suppressed by up to 75% in the presence of antioxidants [1], On the basis of this study we can conclude that reactive oxygen species play an important role in a cytokine-induced activation of PAI-1 expression, and may act as a signal transduction messenger.
3

Inhibition of plasminogen activator inhibitor release in endothelial cell cultures by antisense oligodeoxyribonucleotides with a 5' -end lipophilic modification

75%
Kobylanska A., Pluskota E., Swiatkowska M., Wojcik M., Cierniewska-Cieslak A., Krakowiak A., Boczkowska M., Pawlowska Z., Okruszek A., Koziolkiewicz M., Cierniewski C. S., Stec W. J.
Acta Biochimica Polonica
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1999
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tom 46
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nr 3
A series of conjugates containing residues of lipophilic alcohols covalently bound to 5'-end of oligodeoxyribonucleotides targeted against human plasminogen activator inhibitor (PAI-1) mRNA was synthesized via the oxathiaphospholane approach. The highest anti-PAI-1 activity in EA.hy 926 endothelial cell cultures was found for conjugates containing menthyl or heptadecanyl groups linked with an oligonucleotide complementary to a segment of human PAI-1 mRNA. The phosphodiester antisense oligonucleotides, which otherwise exhibit only limited anti-PAI-1 activity, were found to be more active than phosphorothioate oligonucleotides when conjugated to lipophilic alcohol residues. For menthyl conjugates an evidence of antisense mechanism of inhibition was found.
4

Fibrin D-dimer impairs the accumulation and anticoagulant properties of heparan sulphate and stimulates secretion of plasminogen activator inhibitor-1 by rabbit coronary endothelial cells

75%
Yevdokimova N. Y., Veselovska L. D., Gogolinska G. K., Buchanevich O. M., Kosyakova G. V., Gritsenko P. G., Lugovskoj E. V., Komisarenko S. V.
Acta Biochimica Polonica
|
2003
|
tom 50
|
nr 1
Fibrin split product D-dimer (DD) is most probably involved in the development of vascular disorders. At 1.5 uM concentration DD inhibited the incorporation of D-[1-3H]glucosamine hydrochloride and [2-14C]acetate • Na into pericellular heparan sulphate (HS) of rabbit coronary endothelial cells without affecting other groups of glycosaminoglycans (GAGs). At the same time, DD reduced HS ability to bind antithrombin (AT) and suppressed NO production. The effect of DD on pericellular GAGs was similar to that of Nω-methyl-L-arginine, the competitive inhibitor of endo­thelial NO synthase (eNOS). L-Ascorbic acid, eNOS activator, increased the level of en­dogenous NO in the DD-treated cells, and restored HS accumulation and antithrombin binding. It is suggested that DD influence on endothelial HS may be me­diated by NO production. Another effect of DD, namely, stimulation of plasminogen activator inhibitor-1 (PAI-1) secretion did not depend on the NO level. The decreased HS content, reduced anticoagulant properties of HS, and increased PAI-1 secretion disorganized the endothelial matrix, and promoted fibrin formation and vascular damage. This points to DD as an important factor in the development of vascular disorders.
5
Content available remote

Haemostatic factors and intraluminal thrombus thickness in abdominal aortic aneurysm. Is secondary fibrinolysis relevant?

63%
Siennicka A., Drozdzynska M., Chelstowski K., Cnotliwy M., Jastrzebska M.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 3
6

Plasminogen activator inhibitor-1 [PAI-1] gene 4G-5G promoter polymorphism is not associated with breast cancer

63%
Blasiak J., Smolarz B.
Acta Biochimica Polonica
|
2000
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tom 47
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nr 1
The antigen content of plasminogen activator inhibitor-1 (PAI-1) in primary breast cancer tissue extracts may be of strong prognostic value: high levels of PAI-1 in tumors predict poor prognosis for patients. The gene encoding PAI-1 is highly polymorphic and an insertion (5G)/deletion (4G) polymorphism in the PAI-1 gene promoter (the 4G/5G polymorphism), may have functional significance in PAI-1 expression. In the present work the distribution of genotypes and frequency of alleles of the 4G/5G polymorphism in subjects with breast cancer were investigated. Tumor tissues were obtained from 100 postmenopausal women with node-negative and node-positive ductal breast carcinoma with uniform tumor size. Blood samples from age matched healthy women served as control. The 4G/5G polymorphism was determined by PCR amplification using the allele specific primers. The distribution of the genotypes of the 4G/5G polymorphism in both control and patients did not differ significantly (P > 0.05) from those predicted by the Hardy-Weinberg distribution. There were no differences in the genotype distributions and allele frequencies between node-positive and node-negative patients. The 4G/5G polymorphism may not be linked with elevated level of PAI-1 observed in breast cancer and therefore may not be associated with appearance and/or progression of breast cancer.
7

LAM cells biology and lymphangioleiomyomatosis

51%
Grzegorek I., Drozdz K., Podhorska-Okolow M., Szuba A., Dziegiel P.
Folia Histochemica et Cytobiologica
|
2013
|
tom 51
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nr 1
8
Content available remote

The effect of short term treatment with probiotic VSL#3 on various clinical and biochemical parameters in patients with liver cirrhosis

51%
Marlicz W., Wunsch E., Mydlowska M., Milkiewicz M., Serwin K., Mularczyk M., Milkiewicz P., Raszeja-Wyszomirska J.
Journal of Physiology and Pharmacology
|
2016
|
tom 67
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nr 6
9

Plasminogen activator inhibitor 1 [PAI-1] 1334G-A genetic polymorphism in colorectal cancer

51%
Smolarz B., Romanowicz-Makowska H., Kulig A.
Acta Biochimica Polonica
|
2003
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tom 50
|
nr 2
Plasminogen activator inhibitor 1 (PAI-1) content in colorectal cancer tissue ex­tracts may be of strong prognostic value: high levels of PAI-1 in tumours predict poor prognosis. The gene encoding PAI-1 is highly polymorphic and PAI-1 gene variability could contribute to the level of PAI-1 biosynthesis. In the present work the distribu­tion of genotypes and frequency of alleles of the 1334G/A polymorphism in 92 subjects with colorectal cancer in samples of cancer tissue and distant mucosa samples as well as in blood were investigated. Blood samples age matched healthy individuals (n = 110) served as control. The 1334G/A polymorphism was determined by PCR ampli­fication using allele specific primers. No differences in the genotype distributions and allele frequencies between blood, distant mucosa samples and cancer tissue were de­tected. However, the distribution of the genotypes of the 1334G/A polymorphism in patients differed significantly (P < 0.05) from those predicted by the Hardy-Weinberg equilibrium. There were significant differences in the frequencies of alleles between the colorectal cancer subjects and controls (P < 0.05). The results support the hypothe­sis that the 1334G/A polymorphism may be associated with the incidence of colorectal cancer.
10

Plasminogen activator inhibitor-1 [PAI-1] gene 4G-5G promoter polymorphism in subjects with cancer

51%
Smolarz B., Blasiak J., Piestrzeniewicz D., Pytel J.
Cellular and Molecular Biology Letters
|
1998
|
tom 03
|
nr 1
Plasminogen activator inhibitor PAI-1 is a fast-acting controlling factor of the plasminogen activator system. The system contains proteolytic enzymes that may contribute to cancer cell invasion by degrading the surrounding extracellular matrix and dissociate cell-cell or cell-matrix attachments. There is substantial evidence in many types of cancer that the antigen content of PAI-1 in primary cancer tissue extracts are of strong prognostic value: high level of PAI-1 in tumor predict poor prognosis for the patient. Moreover, it was demonstrated that the level of PAI-1 in metastasis is significantly higher compared to primary tumors. An insertion/deletion polymorphism in the promoter of the PAI-1 gene has been described that relates to plasma PAI-1 levels. We studied this polymorphism in the plasma of subjects with cancer. Blood was taken from 23 patients (10 breast cancers, 5 gastric cancers, 4 head and neck cancers, 2 melanomas and 2 colorectal cancers) and 23 matched controls. Although frequencies of the 4G and 5G alleles were approximately 0.5/0.5 in both patients and controls, the genotype distribution differed significantly between the two groups - the 4G/5G genotype was observed more frequently in patients with cancer than in the controls. Further studies are needed to check whether the prevalence of the 4G/5G genotype may influence an individual’s plasminogen activation system capacity and thereby contribute in a small way to the cancer risk profile.
11
Content available remote

The metabolic syndrome – an ongoing story

45%
Duvnjak L., Duvnjak M.
Journal of Physiology and Pharmacology. Supplement
|
2009
|
tom 60
|
nr 7
12

Concentrations of plasminogen activator inhibitor-1 (PAI-1) and urokinase plasminogen activator (uPA) in induced sputum of asthma patients after allergen challenge

45%
Kowal K., Moniuszko M., Zukowski S., Bodzenta-Lukaszyk A.
Folia Histochemica et Cytobiologica
|
2010
|
tom 48
|
nr 4
13
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Content available

Antithrombotic activity of losartan in two kidney, one clip hypertensive rats. A study on the mechanism of action

45%
Chabielska E., Pawlak R., Wollny T., Rolkowski R., Buczko W.
Journal of Physiology and Pharmacology
|
1999
|
tom 50
|
nr 1
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