Wyniki wyszukiwania - AGRO

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

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2002

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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

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2002

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tom 07

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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

Strain field mapping of the cell membrane of endothelial cells

100%

Feneberg W., Sackmann E.

Cellular and Molecular Biology Letters

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2001

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tom 06

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nr 2

4

[Trans-]endothelial targeting of liposomes in the liver

100%

Scherphof G. L.

Cellular and Molecular Biology Letters

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1999

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tom 04

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nr 2

5

Corneal endothelial cell cultures

88%

Rzymowska J., Gawron A., Swiech-Zubilewicz A., Pawlikowska-Pawlega B.

Folia Histochemica et Cytobiologica. Supplement

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1997

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tom 35

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nr 2

6

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Experimental allogenic transplantation of cornea endothelial cells in cats

75%

Kielbowicz Z., Kuryszko J., Strzadala L.

Polish Journal of Veterinary Sciences

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2010

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tom 13

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nr 4

Background: The aim of the present study was assessing the possibility of experimental allogenic transplantation of cat cornea endothelial cells, multiplied in vitro, into the anterior chamber of the eyeball in recipient cats. The reason for undertaking the research is the need to develop a method that would help in the cornea treatment in animals with corneal opacification following cataract surgery, as well as lens dislocation, injuries and endothelium degeneration. Methods: Cats aged 10-12 months were used in the experiment. Cornea fragments consisting of the posterior limiting membrane and posterior epithelium were placed in Iscove;s medium with addition of 10% foetal calf serum. Multiplied in vitro cells were injected into the anterior chamber of recipient cats. The cornea was subject to histological, histometric and SEM examination on the 3rd, 7th, 20th and 30th day after the surgery. Results: Micromorphological examination of the cornea showed full restitution of its endothelium 30 days after transplantation. Complete regeneration of structures indispensable for normal functioning of the posterior epithelium occurred as a result of implantation. Conclusions: In this study the results show that implantation of the cells of posterior corneal epithelium of donor cats, multiplied into vitro and injected into the anterior chamber of recipient cats. The cornea regained its full function, the layer of the posterior epithelium was regenerated and the stroma stabilized, presenting the image of full and proper corneal translucency.

7

Growth factors and their receptors derived from human amniotic cells in vitro

75%

Grzywocz Z., Pius-Sadowska E., Klos P., Gryzik M., Wasilewska D., Aleksandrowicz B., Dworczynska M., Sabalinska M., Hoser G., Machalinski B., Kawiak J.

Folia Histochemica et Cytobiologica

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2014

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tom 52

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nr 3

8

Plasminogen activator inhibitor type-1 controls the process of the in vitro sprout formation

75%

Chorostowska-Wynimko J., Skrzypczak-Jankun E., Jankun J.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 3

49-56

Plasminogen activator inhibitor type-1 (PAI-1), the primary regulator of plasminogen activator - urokinase (uPA) plays a crucial role in the cell adhesion and migration and in angiogenesis. We had previously demonstrated that PAI-1 - endothelial cell interplay is critical for the formation of new blood vessels and the process is mostly conducted via uPA- anti-proteinase interaction. In the present study we wished to further examine the role of PAI-1 in the sprout formation, representing the first step of new capillary vessels development by evaluating the effect of PAI-1 on the sprout area. We addressed the issue by assessing the influence of cysteine-mutated PAI-1 proteins characterized by a prolonged half-life time (hDßT - T1/2= 63.59 h and ßT- T1/2= 6931.47 h), and therefore more stable anti-uPA activity, on the appearance of newly formed sprouts. We found that both CysPAI-1 proteins significantly diminished the mean sprout area in a concentration-dependent fashion. The inhibitory effect present in the two examined endothelial cells systems of different origin and functional characteristics - human umbilical vein endothelial cells (HUVEC) and human lung microvascular endothelial cells (HLMVEC) cultures - was noticeably greater for HLMVEC -high urokinase-producers. Moreover, the inhibition rate was significantly greater for the ßT mutant than that for the hDßT PAI-1 mutant in all examined doses (P<0.002), proving a key role of anti-proteinase activity for this effect. Therefore, we concluded that PAI-1 apart from the total sprout length affects also sprouts area in the in vitro sprout formation angiogenesis assay. This effect was achieved mainly via PAI-1's anti-proteinase activity.

9

Influence of N-acetylcysteine on ICAM-1 expression and IL-8 release from endothelial and epithelial cells

75%

Radomska-Lesniewska D. M., Sadowska A. M., Van Overveld F. J., Demkow U., Zielinski J., De Backer W. A.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 4

325-334

Chronic obstructive pulmonary disease (COPD) is characterized by chronic airway inflammation. The initial step in the inflammatory process is overexpression of adhesion molecules, which leads to excessive transmigration of neutrophils. One of these adhesion molecules is ICAM-1 which is elevated in COPD patients. In this study we evaluated the influence of N-acetylcysteine (NAC) (0.01 mM-30 mM) on the cytokine-induced (TNF-alphalpha/IL-1ß) expression of the ICAM-1 adhesion molecule and on IL-8 release in endothelial (ECV-304) and bronchial epithelial (H292) cell lines. The methodology used consisted of immunochemistry for the assessment of surface ICAM-1 and ELISA method for that of soluble ICAM-1 and IL-8. NAC inhibited the TNF-alphalpha/IL-1ß-stimulated ICAM-1 expression and IL-8 release from both cell lines in a concentration dependent manner. The most effective concentrations were 30 mM and 20 mM (99 and 90% inhibition respectively, P<0.01). We conclude that NAC is an effective inhibitor of TNF-alphalpha/IL-1ß- stimulated ICAM-1 and IL-8 release in endothelial and epithelial cells. This fact highlights the anti-inflammatory potential of NAC in COPD.

10

Flavonoid transport across RBE4 cells: a blood-brain barrier model

75%

Faria A., Pestana D., Teixeira D., Azevedo J., De Freitas V., Mateus N., Calhau C.

Cellular and Molecular Biology Letters

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2010

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tom 15

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nr 2

There is a growing interest in dietary therapeutic strategies to combat oxidative stress-induced damage to the Central Nervous System (CNS), which is associated with a number of pathophysiological processes, including Alzheimer’s and Parkinson’s diseases and cerebrovascular diseases. Identifying the mechanisms associated with phenolic neuroprotection has been delayed by the lack of information concerning the ability of these compounds to enter the CNS. The aim of this study was to evaluate the transmembrane transport of flavonoids across RBE-4 cells (an immortalized cell line of rat cerebral capillary endothelial cells) and the effect of ethanol on this transport. The detection and quantification of all of the phenolic compounds in the studied samples (basolateral media) was performed using a HPLC-DAD (Diode Array Detector). All of the tested flavonoids (catechin, quercetin and cyanidin-3-glucoside) passed across the RBE-4 cells in a time-dependent manner. This transport was not influenced by the presence of 0.1% ethanol. In conclusion, the tested flavonoids were capable of crossing this blood-brain barrier model.

11

In vitro reoxygenation following hypoxia increases MMP-2 and TIMP-2 secretion by human umbilical vein endothelial cells

75%

Cavdar Z., Oktay G., Egrilmez M. Y., Genc S., Genc K., Altun Z., Islekel H., Guner G.

Acta Biochimica Polonica

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2010

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tom 57

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nr 1

69-73

Endothelial cells lining the inner blood vessel walls play a key role in the response to hypoxia, which is frequently encountered in clinical conditions such as myocardial infarction, renal ischemia and cerebral ischemia. In the present study we investigated the effects of hypoxia and hypoxia/reoxygenation on gelatinases (matrix metalloproteinase-2 and -9), their inhibitor (TIMP-2) and activator (MT1-MMP), in human umbilical vein endothelial (HUVE) cells. HUVE cells were subjected to 4 h of hypoxia or hypoxia followed by 4 and 24 h of reoxygenation. The pro- and active forms of MMP-2 and MMP-9 were analyzed by gelatin zymography; TIMP-2 protein level was assayed using ELISA, while MT1-MMP activity was measured using an activity assay. The secretion of MMP-2 proform increased significantly in cells subjected to 4h of hypoxia followed by 4 or 24 h of reoxygenation, compared with the normoxic group. TIMP-2 protein level also increased significantly in the hypoxia/reoxygenation groups, compared with the normoxic group. There were no statistically significant differences in the levels of active MT1-MMP in all groups. This study indicates that MMP-2 and TIMP-2 could be regarded as important components of a mechanism in the pathophysiology of ischemic injury following reperfusion.

12

Contact of blood and endothelial cells with surface-modified metallic biomaterials

75%

Walkowiak B.

Acta Biochimica Polonica

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2007

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tom 54

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nr Supplement 4

13

Isolation of morphologically and functionally intact gastric mucosal microvessels rapid communication

75%

Tarnawski A., Arakawa T., Sekhon S., Ichikawa Y., Szabo I., Sarfeh I. J.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 1

14

Trans fatty acids induce apoptosis in human endothelial cells

75%

Zapolska-Downar D., Kosmider A., Naruszewicz M.

Journal of Physiology and Pharmacology

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2005

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tom 56

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nr 4

The present study was designed to investigate the hypothesis that trans fatty acids can induce apoptosis of human umbilical vein endothelial cells (HUVEC). To test this hypothesis apoptosis was measured in HUVEC treated with 0.1, 1.0 or 5.0 mM trans elaidic acid (t-18:1) or linoelaidic acid (t,t-18:2) for 24 hours. For the detection of apoptosis, TdT-mediated dUTP nick end labelling assay (TUNEL), cell binding of annexin V and propidium iodide uptake were measured. Active Caspase-3 and cleaved PARP (poly-ADP-ribose polymerase) were also measured in the cell lysate. Moreover, cellular ability to produce ROS (reactive oxygen species) was measured by DCF fluorescence Both acids studied induce both early (annexin-positive cells) and late stages of apoptosis (cells stained by propidium iodide) in a dose-dependent manner. Also the appearance of TUNEL-positive cells was induced by both trans fatty acids tested, in a dose dependent manner. Both trans acids induce apoptosis through their effect on Caspase-3 activity and on intracellular ROS production. It is worth emphasising that linoelaidic acid proved to be a more potent inducer of apoptosis and ROS production in endothelial cells than elaidic acid. The present studies suggest that trans fatty acids may play a role in damaging and death of vascular endothelial cells in atherosclerosis.

15

Inhibition of hypoxia-induced tolerance to subsequent hyperoxic injury in lung cells by phosphatidyl inositol 3-kinase inhibitors: LY294002 and wortmannin

75%

Ahmad S., Ahmad A., Gerasmivoskaya E., Stenmark K. R., White C. W.

Cellular and Molecular Biology Letters

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2003

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tom 08

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nr 2A

16

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

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2003

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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.

17

Distribution of NADPH-diaphorase activity in the pineal gland of the turkey

75%

Lewczuk B., Nowicki M., Brzozowski W., Przybylska-Gornowicz B.

Folia Histochemica et Cytobiologica

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2002

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tom 40

|

nr 2

18

Interleukin 1beta induces functional prostaglandin E synthase in cultured human umbilical vein endothelial cells

75%

Uracz W., Uracz D., Olszanecki R., Gryglewski R. J.

Journal of Physiology and Pharmacology

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2002

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tom 53

|

nr 4,1

Prostaglandin endoperoxide H2 (PGH2) is generated from arachidonic acid by either constitutive (COX-1) or inducible (COX-2) cyclooxygenases. In arterial wall PGH2 is converted by PGI2 synthase (PGI-S) to prostacyclin (PGI2), and in platelets by thromboxane synthase (TX-S) to thromboxane (TXA2). Other prostanoids as PGD2, PGF2alpha or PGE2 were believed to arise non-enzymatically from PGH2. Only recently, human prostaglandin E synthase (PGE-S) has been identified and cloned as a membrane bound, microsomal, glutathione-dependent inducible enzyme. Here we demonstrated that interleukin 1ß (IL-1ß) is an inducer of COX-2 and PGE-S in human umbilical vein endothelial cells (HUVEC). Functional expression of PGE-S was measured at the level of specific mRNA by semi-quantitative RT-PCR, PGE-S protein was detected by Western blot in HUVEC, while PGE2 was measured by immunoassay in the supernatant. Actinomycin D, a classical transcription inhibitor, was used to prove that indeed IL-1ß induced the functional PGE-S enzyme. PGE2 generation in HUVEC was inhibited by indomethacin, acetamoniphen and dexamethasone. In conclusion, we found that in cultured endothelial cells IL-1ß induced as evidenced by the appearance of its transcript and its functional enzyme. The induction of endothelial PGE-S and COX-2 appeared to be and their transcripts were induced as fast as one might expect from immediate early genes. It means that IL-1ß-triggered-PGE2 biosynthesis in endothelial cells is probably regulated by induction of both COX-2 and PGE-S. This is way we hypothesise the existence of at least two distinct pools of COX-2: the first selectively coupled to PGE-S and the second one that is coupled to PGI-S yielding the main endothelial product - PGI2.

19

Morphological changes in endothelial cells of uterine artery of cycling and ovariectomized-estradiol treated ewes

75%

Zezula-Szpyra A., Gawronska B., Skipor J.

Folia Morphologica

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1996

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tom 55

|

nr 4

20

Influence of TNF-alpha and-or zinc, magnesium on collagen metabolism in the culture of porcine endothelial cells

75%

Skop B., Grabowska-Bochenek R., Kotrys-Puchalska E., Dec R., Sobczak A., Drozdz M.

Folia Histochemica et Cytobiologica. Supplement

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1997

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tom 35

|

nr 2

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