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1
Content available remote

Beta-carotene and arachidonic acid induced DNA methylation and the regulation of pro-chemotactic activity of endothelial cells and its progenitors

100%
Kiec-Wilk B., Polus A., Mikolajczyk M., Mathers J. C.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 4
DNA methylation is one of the important mechanisms regulating gene expression. Since beta-carotene (BC) was shown to have pro-chemotactic activity and stimulates expression of pro-angiogenic genes, this study was undertaken to define the possible changes in DNA methylation in endothelial cell and its progenitors in the presence of BC. The culture medium for human umbilical vein endothelial cells (HUVEC) and endothelial progenitor cells (EPC) was supplemented with BC (1 - 10 µM) with the presence of arachidonic acid (AA) (3 µM). Global DNA methylation tended to be lower in both endothelial cell lines, after incubation with BC and AA. HUVEC incubated with AA demonstrated the lowest DNA methylation. The decrease of DNA methylation in EPC, induced by BC, was concentration - dependent. The microarray study revealed, that the angiogenesis and homing – related genes were mostly influenced by BC and AA in investigated cells. Our results indicate that BC and AA-induced DNA hypomethylation in EPC and HUVEC, might be a mechanism which may alter gene expression in endothelial cells what in certain conditions may be connected with the suggested pro-malignant effect of this compounds.
2

The chemotactic activity of beta-carotene in endothelial cell progenitors and HUVEC. The microarray analysis

88%
Polus A., Hartwich J., Kiec-Wilk B., Mikolajczyk M., Dembinska-Kiec A.
Acta Biochimica Polonica
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2007
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tom 54
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nr Supplement 4
3

Differentiation of human adipose tissue progenitors to adipocytes or endothelial cells using different culture conditions

88%
Balwierz A., Czech U., Polus A., Dudek W., Dembinska-Kiec A.
Acta Biochimica Polonica
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2007
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tom 54
|
nr Supplement 4
4

CpG islands methylation induced by betacarotene and arachidonic acid in human endothelial cells and its progenitors

76%
Kiec-Wilk B., Polus A., Mikolajczyk M., Hartwich J., Mathers J., Dembinska-Kiec A.
Acta Biochimica Polonica
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2007
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tom 54
|
nr Supplement 4
5
Content available remote

The MAPK-dependent regulation of the Jagged/Notch gene expression by VEGF, bFGF or PPAR gamma mediated angiogenesis in HUVEC

76%
Kiec-Wilk B., Grzybowska-Galuszka J., Polus A., Pryjma J., Knapp A., Kristiansen K.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 2
The Jagged-Notch signalling, plays a crucial role in cell differentiation. Angiogenesis, is regulated by VEGF, bFGF as well as by the free fatty acid metabolites , which are regulators of transcription factors such as peroxisome proliferation activating receptors (PPARs). The study analyzed the signalling pathways involved in the regulation of Jagged-1/Notch-4 expression in endothelial cells (HUVECs) in response to VEGF, bFGF and PPAR- exogenous activator - ciglitazone. HUVECs were incubated with investigated substances for 24 hours, with or without the presence of the MAP-kinases inhibitors were used. Jagged-1 and Notch-4 gene expression was determined using quantitative Real-Time PCR. The Jagged-1/Notch-4 protein expression was compared by flow cytometry, when the phosphorylation-dependent activation of kinases was estimated by Western-blot method. The opposite effect of VEGF, bFGF, or ciglitazone on the Jagged-1/Notch-4 expression on HUVEC was connected with the different activation of MAPKs. Ciglitazone, activated p38 MAPK pathway and simultaneously inhibited phosphorylation of p42/44 MAPK. The pro-angiogenic: bFGF and VEGF, also activated the p38 MAPK, but they did not attenuate the p42/44 MAPK phosphorylation. Maintaining of the Jagged/Notch interactions by VEGF, when down-regulation by bFGF and ciglitazone, seems to be dependent on the different effect on p38 MAPK and p42/44 MAPK pathway regulation.
6

Modulation of the human preadipocyte mitochondrial activity by beta-carotene

76%
Sliwa A., Goralska J., Czech U., Gruca A., Polus A., Zapala B., Dembinska-Kiec A.
Acta Biochimica Polonica
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2012
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tom 59
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nr 1
 Increased ROS generation by the overload by metabolic substrates mitochondria paralleled by decrease of antioxidant activity are typical events found in metabolic syndrome and diabetes type 2. Metabolites of beta-carotene (BC) such as retinoic acid (RA), as well as low concentration of reactive oxygen species (ROS) modify the mitochondrial bioenergetic function. The aim of the study was to investigate the effect of beta-carotene on mitochondrial activity in human preadipocytes. BC used in concentrations, 10 or 30 µM, decreased mitochondrial membrane potential, inhibited mitochondrial respiration and decreased cellular ATP content. We conclude, that BC, the known antioxidant may decrease oxidative phosphorylation capacity of mitochondria.
7

Action of pyrethroids on different levels of insect nervous system

76%
Ciolek J., Kielbasiewicz E., Polus A., Kadziela W., Pelhate M., Stankiewicz M.
Pestycydy
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2005
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nr 3
169-176
8
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Content available

Regulation of inducible nitric oxide synthase [iNOS] and GTP cyclohydrolase I [GTP-CH I] gene expression by OX-LDL in rat vascular smooth muscle cells

76%
Dulak J., Polus M., Guevara I., Polus A., Hartwich J., Dembinska-Kiec A.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 4
9

Animal models of human metabolic syndrome and pathological angiogenesis

64%
Wator L., Razny U., Polus A., Stachura J., Dyduch G., Wan Y., Joost H.-G., Dembinska-Kiec A.
Acta Biochimica Polonica
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2007
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tom 54
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nr Supplement 4
10

The human immunodeficiency virus (HIV1) protease inhibitor sanquinavir activates autophagy and removes lipids deposited in lipid droplets

64%
Polus A., Bociaga-Jasik M., Czech U., Goralska J., Cialowicz U., Chojnacka M., Polus M., Jurkowski K., Dembinska-Kiec
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 2
11

Glucagon-like peptide-1 receptor agonist stimulates mitochondrial bioenergetics in human adipocytes

64%
Goralska J., Sliwa A., Gruca A., Razny U., Chojnacka M., Polus A., Solnica B., Malczewska-Malec M.
Acta Biochimica Polonica
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2017
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tom 64
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nr 3
12
Content available remote

The adipose tissue gene expression in mice with different nitric oxide availability

64%
Razny U., Kiec-Wilk B., Polus A., Wator L., Dyduch G., Partyka L., Bodzioch M., Tomaszewska R., Wybranska I.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 5
Mice with the knockout of endothelial nitric oxide synthase (eNOS ko) demonstrate symptoms resembling the human metabolic syndrome. NO has been recently demonstrated to be deeply involved in regulation of not only blood flow and angiogenesis, but also in modulation of mammalian basal energy substrate metabolism. Asymmetric dimethylarginine (ADMA) is an endogenous competitive inhibitor of NOS. The enzyme dimethylarginine dimethylaminohydrolase (DDAH) catabolizes ADMA, what leads to increase of endogenous NO bioavailability. This study was aimed to compare the brown (BAT) and white (WAT) adipose tissue gene expression of age matched mice with decreased (eNOS ko) and increased (overexpressing DDAH) endogenous NO generation. The 19 week old eNOS ko mice demonstrated significantly lower weight, higher circulating glucose, insulin, leptin and cholesterol concentrations. The adiponectin as well as fasting triglyceride concentrations were not significantly altered. Animals with DDAH knock in, presented significantly increased angiogenic activity than eNOS ko mice. The microarray analysis pointed to activation of adipogenesis-related genes in eNOS ko mice in WAT, what was in contrast with the inhibition observed in the DDAH overexpressing mice. The angiogenesis related gene expression was down-regulated in both models in comparison to WT animals. This study support the multipotential role of endogenous NO in maintaining homeostasis of energy substrate catabolism.
13
Content available remote

Influence of ghrelin on gastric and duodenal growth and expression of digestive enzymes in young mature rats

52%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Cieszkowski J., Konturek S. J., Polus A., Pawlik W. W., Kuwahara A., Kato I., Konturek P. C.
Journal of Physiology and Pharmacology
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2006
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tom 57
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nr 3
Ghrelin, a nature ligand for the growth hormone secretagogue receptor (GHS-R), stimulates a release of growth hormone, prolactin and adrenocorticotropic hormone. Also, ghrelin increases food intake in adult rats and humans and exhibits gastroprotective effect against experimental ulcers induced by ethanol or stress. The aim of present study was to examine the influence of ghrelin administration on gastric and duodenal growth and expression of pepsin and enterokinase in young mature rats with intact or removed pituitary. Methods: Two week after sham operation or hypophysectomy, eight week old Wistar male rats were treated with saline (control) or ghrelin (4, 8 or 16 nmol/kg/dose) i.p. twice a day for 4 days. Expression of pepsin in the stomach and enterokinase in the duodenum was evaluated by real-time PCR. Results: In animals with intact pituitary, treatment with ghrelin increased food intake, body weight gain and serum level of growth hormone and insulin-like growth factor-1 (IGF-1). These effects were accompanied with stimulation of gastric and duodenal growth. It was recognized as the significant increase in gastric and duodenal weight and mucosal DNA synthesis. In both organs, ghrelin administered at the dose of 8 nmol/kg caused maximal growth-promoting effect. In contrast to these growth-promoting effects, administration of ghrelin reduced expression of mRNA for pepsin in the stomach and was without effect on expression of mRNA for enterokinase in the duodenum. Hypophysectomy alone lowered serum concentration of growth hormone under the detection limit and reduced serum level of IGF-1 by 90%. These effects were associated with reduction in daily food intake, body weight gain and gastroduodenal growth. In hypophysectomized rats, administration of ghrelin was without significant effect on food intake, body weight gain or growth of gastroduodenal mucosa. Also, serum concentration of growth hormone or IGF-1 was not affected by ghrelin administration in rats with removed pituitary. Conclusion: Administration of ghrelin stimulates gastric and duodenal growth in young mature rats with intact pituitary, but inhibits expression of mRNA for pepsin in the stomach. Growth hormone and insulin-like growth factor-1 play an essential role in growth-promoting effects of ghrelin in the stomach and duodenum.
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