Wyniki wyszukiwania

1

Structure and physiological functions of the human peroxisome proliferator-activated receptor gamma

100%

Zieleniak A., Wojcik M., Wozniak L. A.

Archivum Immunologiae et Therapiae Experimentalis

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2008

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tom 56

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nr 5

2

The role of peroxisome-proliferator-activating receptor gamma agonists: rosiglitazone and 15-deoxy-delta12,14-prostaglandin J2 in chronic experimental cyclosporine A-induced nephrotoxicity

84%

Korolczuk A., Maciejewski M., Smolen A., Dudka J., Czechowska G., Widelska I.

Journal of Physiology and Pharmacology

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2014

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tom 65

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nr 6

3

Ligands of peroxisome proliferator-activated receptor-gamma increase the generation of vascular endothelial growth factor in vascular smooth muscle cells and in macrophages

84%

Jozkowicz A., Dulak J., Piatkowska E., Placha W., Dembinska-Kiec A.

Acta Biochimica Polonica

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2000

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tom 47

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nr 4

Peroxisome proliferator-activated receptors-gamma (PPARgamma) are ligand-inducible transcription factors of the nuclear hormone receptor superfamily. We examined the effect of PPARgamma activation on the generation of vascular endothelial growth factor (VEGF), one of the major angiogenic agents. Rat vascular smooth muscle cells (VSMC) and murine macrophages RAW264.7 were incubated for 24 h with PPARgamma activators: prostaglandin J2 and ciglitazone. PPARgamma were expressed in VSMC and RAW cells and their activity was upregulated in the presence of PGJ2 and ciglitazone. Incubation of the cells with PPARgamma activators significantly augmented the release of VEGF protein into the media, both in resting and in IL-1beta- or LPS-stimulated cultures. The higher protein generation was connected with the increased expression of mRNA and transcriptional activation of VEGF promoter. We conclude that the activation of PPARgamma upregulates the generation of VEGF and may be involved in the regulation of angiogenesis.

4

Pioglitazone, a PPAR-gamma ligand, exerts cytostatic-cytotoxic effects against cancer cells, that do not result from inhibition of proteasome

84%

Mrowka P., Glodkowska E., Mlynarczuk-Bialy I., Bialy L., Kuckelkorn U., Nowis D., Makowski M., Legat M., Golab J.

Acta Biochimica Polonica

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2008

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tom 55

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nr 1

Thiazolidinediones are oral antidiabetic agents that activate peroxisome proliferator-activated receptor-gamma (PPAR-γ) and exert potent antioxidant and anti-inflammatory properties. It has also been shown that PPAR-γ agonists induce G0/G1 arrest and apoptosis of malignant cells. Some of these effects have been suggested to result from inhibition of proteasome activity in target cells. The aim of our studies was to critically evaluate the cytostatic/cytotoxic effects of one of thiazolidinediones (pioglitazone) and its influence on proteasome activity. Pioglitazone exerted dose-dependent cytostatic/cytotoxic effects in MIA PaCa-2 cells. Incubation of tumor cells with pioglitazone resulted in increased levels of p53 and p27 and decreased levels of cyclin D1. Accumulation of polyubiquitinated proteins within cells incubated with pioglitazone suggested dysfunction of proteasome activity. However, we did not observe any influence of pioglitazone on the activity of isolated proteasome and on the proteolytic activity in lysates of pioglitazone-treated MIA PaCa-2 cells. Further, treatment with pioglitazone did not cause an accumulation of fluorescent proteasome substrates in transfected HeLa cells expressing unstable GFP variants. Our results indicate that pioglitazone does not act as a direct or indirect proteasome inhibitor.

5

Comparison of the anti-inflammatory and therapeutic actions of PPAR-gamma agonists rosiglitazone and troglitazone in experimental colitis

67%

Celinski K., Dworzanski T., Fornal R., Korolczuk A., Madro A., Slomka M.

Journal of Physiology and Pharmacology

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2012

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tom 63

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nr 6

6

Effects of pioglitazone and high-fat diet on ceramide metabolism in rat skeletal muscles

67%

Zendzian-Piotrowska M., Baranowski M., Zabielski P., Gorski J.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

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nr 10

101-114

Ceramide is involved in the pathogenesis of insulin resistance in skeletal muscles of humans and rodents. However, there are conflicting reports in the literature on the effect of thiazolidinediones (a new class of insulin sensitizing drugs) on skeletal muscle ceramide content. Therefore, the aim of our study was to examine the effect of pioglitazone on the level of ceramide and its metabolites and on the activity of the key enzymes of ceramide metabolism in different skeletal muscle types of the rat. The experiments were carried out on rats fed either a standard chow or a high-fat diet for 21 days. Each group was divided into two subgroups: control and treated with pioglitazone for 14 days. High-fat diet increased the content of ceramide in the soleus and in the red section of the gastrocnemius, but not in the white section of the latter. The activity of neutral Mg2+-dependent sphingomyelinase and acid sphingomyelinase was simultaneously reduced in all examined muscles. Administration of pioglitazone decreased ceramide level in the soleus and in the red section of the gastrocnemius in rats fed either diet. This effect could not be attributed to decreased rate of ceramide formation from sphingomyelin or to its augmented deacylation to sphingosine. Pioglitazone treatment reduced the concentration of plasma free fatty acids in rats fed on either diet. Therefore, we conclude that the drug decreased the muscle content of ceramide by reducing its de novo synthesis. The results of our study indicate that reduction in ceramide level may be one of the mechanisms by which pioglitazone improves skeletal muscle insulin sensitivity.

7

Therapy of nonalcoholic fatty liver disease: current status

51%

Duvnjak M., Tomasic V., Gomercic M., Smircic Duvnjak L., Barsic N., Lerotic I.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

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nr 7