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  1. 10 Journal of Physiology and Pharmacology

  2. 2 Acta Biochimica Polonica

  3. 1 Cellular and Molecular Biology Letters

  4. 1 Folia Histochemica et Cytobiologica

  5. 1 Journal of Physiology and Pharmacology. Supplement

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  1. 2 Bogacka I.

  2. 2 Bogacki M.

  3. 2 Chabowski A.

  4. 2 Chojnowska K.

  5. 2 Gonciarz M.

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  1. 1 2018

  2. 1 2017

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  4. 3 2014

  5. 2 2013

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1
Content available remote

Metabolic modulators of the exercise response: doping control analysis of an agonist of the peroxisome proliferator-activated receptor delta (GW501516) and 5-aminoimidazole- 4-carboxamide ribonucleotide (AICAR)

100%
Pokrywka A., Cholbinski P., Kaliszewski P., Kowalczyk K., Konczak D., Zembron-Lacny A.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 4
2
Content available remote

Differential effects of in vivo PPAR alpha and gamma activation on fatty acid transport proteins expression and lipid content in rat liver

86%
Wierzbicki M., Chabowski A., Zendzian-Piotrowska M., Gorski J.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 1
99-106
Peroxisome proliferator-activated receptors (PPAR`s) serve as lipid sensors and when activated modify gene expression of proteins highly involved in the regulation of fatty acid metabolism. Recently, the accumulation of lipids in liver was shown to be depended on the excessive protein-mediated transmembrane transport of long chain fatty acids (LCFAs). The aim of the present study was to determine the in vivo effects of PPAR and activation at two levels: 1) on the expression of fatty acid transporters, 2) on the content and fatty acids saturation status of lipids in rats liver. PPAR agonist (WY 14,643) treatment upregulated the liver expression of FAT/CD36 (+20%, p<0.05) and did not significantly affect the content of FABPpm and FATP-1. Accordingly there was a significant increase in the content of phospholipid (+12%, p<0.05), diacylglycerol (+65%, p<0.05) and triacylglycerol (+46%, p<0.05) fractions followed PPAR activation. In contrast, pioglitazone (PPAR agonist) had no effect on the content of fatty acid transporters (FAT/CD36, FABPpm and FATP-1) as well as the content of liver lipid fractions with the exception for triacylglycerols, which have been reduced significantly (-89%, p<0.05). These findings suggest that in vivo PPAR and PPAR activation exert different effects on both the expression of fatty acid transporters and lipid content in rat’s liver.
3
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Peroxisome proliferator activated receptor ligands affect progesterone and 17beta-estradiol secretion by porcine corpus luteum during early pregnancy

86%
Kurzynska A., Bogacki M., Chojnowska K., Bogacka I.
Journal of Physiology and Pharmacology
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2014
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tom 65
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nr 5
4

The PPAR alpha pathway in V gamma 9V delta 2 T cell anergy

86%
Poupot M., Boissard F., Betous D., Bardouillet L., Fruchon S., L Faqihi-olive F., Pont F., Mekaouche M., Ingoure S., Sicard H., Dubreuilh G., Fournie J.-J.
Cellular and Molecular Biology Letters
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2014
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tom 19
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nr 4
Phosphoantigens (PAgs) activate Vγ9Vδ2 T lymphocytes, inducing their potent and rapid response in vitro and in vivo. However, humans and nonhuman primates that receive repeated injections of PAgs progressively lose their Vγ9Vδ2 T cell response to them. To elucidate the molecular mechanisms of this in vivo desensitization, we analyzed the transcriptome of circulating Vγ9Vδ2 T cells from macaques injected with PAg. We showed that three PAg injections induced the activation of the PPARα pathway in Vγ9Vδ2 T cells. Thus, we analyzed the in vitro response of Vγ9Vδ2 T cells stimulated with a PPARα agonist. We demonstrated that in vitro PPARα pathway activation led to the inhibition of the BrHPP-induced activation and proliferation of human Vγ9Vδ2 T cells. Since the PPARα pathway is involved in the antigen-selective desensitization of human Vγ9Vδ2 T cells, the use of PPARα inhibitors could enhance cancer immunotherapy based on Vγ9Vδ2 T cells.
5
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The selected pathophysiological aspects of PPARs activation

86%
Kiec-Wilk B., Dembinska-Kiec A., Olszanecka A., Bodzioch M., Kawecka-Jaszcz K.
Journal of Physiology and Pharmacology
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2005
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tom 56
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nr 2
Peroxisome proliferator activated receptors (PPARs) belong to a subfamily of transcription nuclear factors. Three isoforms of PPARs have been identified: alpha, ß/ and , encoded by different genes and distributed in various tissues. They play important roles in metabolic processes like regulation of glucose and lipid redistribution. They also have anti-atherogenic, anti-inflammatory as well as anti-hypertensive functions. In hypertension-induced cardiac hypertrophy, both PPARalpha and PPAR activation reveal cardio-protective effect. Despite these beneficial functions, several recent experimental reports point to the possibille unfavorable effects of PPARs activation in lipid metabolism (lipotoxicity) in cardiomyocytes, which can lead to pathologic cardiac hypertrophy in such diseases as diabetes type 2, metabolic syndrome or obesity. This paper reviews evidences and hypotheses about the new pathophysiological aspects of PPARs activation.
6
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Only live Helicobacter pylori is capable of caspase-3 dependent apoptosis induction in gastric mucosa epithelial cells

72%
Pierzchalski P., Pytko-Polonczyk J., Jaworek J., Konturek S. J., Gonciarz M.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 4
119-128
Physiological process of cell death, apoptosis, plays a beneficial role in organism survival, but in some pathologies, like gastric Helicobacter pylori (Hp) infection, this process may turn against the host organism causing tissue damage. Knowledge of the mechanisms controlling apoptosis may have potential significance in treatment of these pathologic states. Therefore, we sought to determine whether apoptosis induced in the gastric epithelial cells exposed to live Hp involves the alteration in heat shock protein 70 (HSP70) expression and activation of caspase-3 in peroxisome proliferator-activated receptors (PPARg dependent manner). Experiments were performed with KATO III, gastric epithelial cells, exposed to CagA and Vac A positive live Hp , water Hp extracts or Hp culture supernatant over different time periods. Total cellular RNA and proteins were isolated for PCR, western-blot and EMSA studies. Genomic DNA was isolated to analyze apoptosis status. We propose new model of Hp induced HSP70 dependent, caspase-3 executed apoptosis in human gastric epithelium. KATO III cells exposed to Hp , showed an increase in caspase-3 activity accompanied and preceeded by activation of nuclear translocation of PPAR peaking at 48 h of culture. Moreover, heat shock factor 1 (HSF-1) bound up with phosphorylated STAT-3 was unable to activate HSP70 protein synthesis in KATO III exposed to Hp . Lack of protective effect of HSP70, activation of caspase-3 - dependent apoptosis pathway caused by Hp and alteration of the bax/bcl-2 cellular equilibrium led to gastric epithelial cell death. The observed phenomenon might be helpful in understanding of the mechanism of Hp related gastrointestinal tract diseasess, especially gastric cancer.
7
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Liver X receptor agonist T0901317 enhanced peroxisome proliferator-activated receptor-delta expression and fatty acid oxidation in rat skeletal muscle

72%
Baranowski M., Blachnio-Zabielska A. U., Zabielski P., Harasim E., Harasiuk D., Chabowski A., Gorski J.
Journal of Physiology and Pharmacology
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2013
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tom 64
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nr 3
8
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Content available

Regulation of steroidogenic function of mouse Leydig cells: G-coupled membrane estrogen receptor and peroxisome proliferator-activated receptor partnership

72%
Gorowska-Wojtowicz E., Dutka P., Kudrycka M., Pawlicki P., Milon A., Plachno B. J., Tworzydlo W., Pardyak L., Kaminska A., Hejmej A., Bilinska B., Kotula-Balak M.
Journal of Physiology and Pharmacology
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2018
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tom 69
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nr 3
9
Content available remote

Expression of peroxisome proliferator-activated receptors is regulated by gonadotropins and steroid hormones in in vitro porcine ovarian follicles

72%
Kurowska P., Chmielinska J., Ptak A., Rak A.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 6
10

Evidence for differential effects of glucose and cycloheximide on mRNA levels of peroxisome proliferator-activated receptor- (PPAR-) machinery members: Superinduction of PPAR-gamma1 and -gamma2 mRNAs

72%
Rypka M., Vesely J.
Acta Biochimica Polonica
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2010
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tom 57
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nr 2
 Quantitative real-time RT-PCR study was conducted to reveal the effects of normal (5 mmol/l) and high (30 mmol/l) glucose without or with oleate (0.3 mmol/l) on mRNA levels of peroxisome proliferator-activated receptor- (PPAR-)α, -γ1, -γ2, and peroxisome proliferator-activated receptor-γ coactivator- (PGC-)1α and -1β in commercial human hepatoma-derived HepG2 cells maintained under low-serum condition. Significant decrease in PPAR-γ1 and PGC-1α mRNA levels to about 50 % was observed during the first 4 h incubation period. During the next 4 h period, both PPAR-γ1 and PGC-1α mRNAs were partly but significantly restored in high glucose batches. In this period, the presence of the transcriptional inhibitor actinomycin D revealed a significant protective effect of excess glucose on mature PPAR-γ1 and PGC-1α mRNAs. Furthermore, PPAR-γ1 and -γ2 mRNAs were differentially superinduced 1.2-2.5 fold in cells upon the administration of the translational inhibitor cycloheximide. When the cells were co-treated with the combination of cycloheximide and actinomycin D, superinduction was completely suppressed, however. Altogether, the experiments revealed, first, an unexpected protective effect of abundant glucose on PPAR-γ1 and PGC-1α mRNAs in HepG2 cells. Second, we demonstrated cycloheximide-induced, transcription-dependent upregulation of mature PPAR-γ1 and -γ2 mRNAs in HepG2 cells associated with preferential expression of the PPAR-γ2 mRNA variant. The results draw attention to as yet unexplored mechanisms involved in the control of PPAR and PGC genes.
11

Polymorphic variants of the PPAR (Peroxisome Proliferator-Activated Receptor) genes: relevance for athletic performance

72%
Maciejewska-Karlowska A.
Trends in Sport Sciences
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2013
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tom 20
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nr 1
The elite athletic phenotype is a complex combination influenced by both multiple genes (polygenic) and environmental factors such as training and nutrition. Among single nucleotide polymorphisms (SNPs) associated with variation in physical traits, which are particularly important for performance in a variety of sports and with the elite athlete status, variants of PPAR (Peroxisome Proliferator-Activated Receptor) genes have emerged as crucial moderators that control the expression of genes encoding enzymes and other proteins involved in energy homeostasis (lipid and carbohydrate metabolism). Accumulated findings from studies showing that combinations of polymorphic markers located in PPAR genes are associated with increased/decreased performance raise the possibility that the PPAR gene variants are true performance enhancing polymorphisms (PEPs) that are believed to have a physiological impact on human body composition and metabolism. The aim of this review is to summarize the state of knowledge on the role of polymorphic variants of PPAR genes in physical performance or health related fitness phenotypes.
12

Conjugated linoleic acids regulate triacylglycerol and cholesterol concentrations in macrophages/foam cells by the modulation of CD36 expression

58%
Stachowska E., Baskiewicz M., Marchlewicz M., Czuprynska K., Kaczmarczyk M., Wiszniewska B., Machalinski B., Chlubek D.
Acta Biochimica Polonica
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2010
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tom 57
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nr 3
Atherosclerosis is an inflammatory disease characterised by the accumulation of lipids and their metabolites in the artery wall. During inflammation circulating LDL are taken up by macrophages through two major scavenger receptors: CD36 and scavenger receptor A (SRA). Fatty acids that are common in food, e.g. linoleic acid and n-3 unsaturated fatty acids can modulate expression of CD36 on the macrophage surface. Conjugated linoleic acid isomers (CLA) that originate from the human diet, have demonstrated antiatherogenic properties in several experiments. Animal study evidenced that CLA could induce resolution of plaque by activation of peroxisome proliferator activated receptors and down-regulation of pro-inflammatory genes. Less unequivocal results were obtained in human studies (on the CLA effects on the inflammatory process). Therefore in this study we investigated the influence of CLA on CD36 expression and lipid accumulation in human macrophages. Macrophages were incubated with 30 µM cis-9,trans-11 CLA, trans-10,cis-12 CLA or linoleic acid for 48 h. After that, expression of CD36 as well as accumulation of lipids were measured by flow cytometry, microscopy and a spectroscopic method. We demonstrate that both cis-9,trans-11 C 18 : 2 CLA and linoleic acid slightly elevated expression of CD36, whereas second isomer - trans-10,cis-12 CLA - did not. Nevertheless, only trans-10,cis-12 CLA triggered delipidation of macrophages, that is decreased triacylglycerols concentration. Also in human adipocytes, trans-10,cis-12 CLA causes cell delipidation by reduction of PPAR receptor expression. We propose a similar mechanism for human macrophages/foam cells.
13
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The MAPK-dependent regulation of the Jagged/Notch gene expression by VEGF, bFGF or PPAR gamma mediated angiogenesis in HUVEC

58%
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.
14

Peroxisome proliferator-activated receptors in the regulation of female reproductive functions

58%
Bogacka I., Kurzynska A., Bogacki M., Chojnowska K.
Folia Histochemica et Cytobiologica
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2015
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tom 53
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nr 3
15
Content available remote

Prominent role of liver in elevated plasma palmitoleate levels in response to rosiglitazone in mice fed high-fat diet

58%
Kuda O., Stankova B., Tvrzicka E., Hensler M., Jelenik T., Rossmeisl M., Flachs P., Kopecky J.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 4
135-140
In humans, antidiabetics thiazolidinediones (TZDs) upregulate stearoyl-CoA desaturase 1 (SCD1) gene in adipose tissue and increase plasma levels of Scd1 product palmitoleate, known to enhance muscle insulin sensitivity. Involvement of other tissues in the beneficial effects of TZDs on plasma lipid profile is unclear. In our previous study in mice, in which lipogenesis was suppressed by corn oil-based high-fat (cHF) diet, TZD rosiglitazone induced hepatic Scd1 expression, while liver triacylglycerol content increased, VLDL-triacylglycerol production decreased and plasma lipid profile and whole-body glycemic control improved. Aim of this study was to characterise contribution of liver to changes of plasma lipid profile in response to a 8-week-treatment by rosiglitazone in the cHF diet-fed mice. Rosiglitazone (10 mg/kg diet) upregulated expression of Scd1 in various tissues, with a stronger effect in liver as compared with adipose tissue or skeletal muscle. Rosiglitazone increased content of monounsaturated fatty acids in liver, adipose tissue and plasma, with palmitoleate being the most up-regulated fatty acid. In the liver, enhancement of Scd1 activity and specific enrichment of cholesteryl esters and phosphatidyl cholines with palmitoleate and vaccenate was found, while strong correlations between changes of various liver lipid fractions and total plasma lipids were observed (r=0.74-0.88). Insulin-stimulated glycogen synthesis was increased by rosiglitazone, with a stronger effect in muscle than in liver. Conclusions: changes in plasma lipid profile favouring monounsaturated fatty acids, mainly palmitoleate, due to the upregulation of Scd1 and enhancement of Scd1 activity in the liver, could be involved in the insulin-sensitizing effects of TZDs.
16
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Molecular mechanism of protection against chemically and gamma-radiation induced apoptosis in human colon cancer cells

58%
Pierzchalski P., Krawiec A., Gawelko J., Pawlik W. W., Konturek S. J., Gonciarz M.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 2
The involvement of peroxisome proliferator-activated receptors (PPARs) in the cancer cell elimination through apoptosis is a generally accepted fact. However, some reports indicate that the activation of PPAR is directly responsible for carcinogenesis. Caco-2 cells, a human adenocarcinoma cells, were used as a model of colon cancer. Cell cultures (5x106 cell per dish) were pretreated for 24h with PPARagonists ciglitazone (CI, 1x10-6M) and retinoic acid (RA, 1x10-6M) and part of the cultures were subsequently subjected to -radiation (photons) with therapeutic dose of 2,5 Gy. Total cellular RNA and proteins (cytoplasmic and nuclear) were isolated 24h after cultures irradiation or 48h after stimulation in the non irradiated part of experiment to preserve the equal growth time for all samples. -Irradiation of the cells abolished nuclear translocation of PPARunder its agonists treatment and preserved PPARin the cytoplasmic pool. But it did not affect the HSP 70 expression in response to ciglitazone and retinoic acid. Moreover, combined -irradiation and CI/RA treatment of the cells changed the equilibrium between Bax and Bcl-2 mRNA to anti apoptotic state with increased expression of Bcl-2 and almost abolished expression of Bax. In conclusion, this paper provides an evidence for the anti-apoptotic action of PPARagonists used along with the -radiation. Moreover, it shows that the up-regulated HSP70, in response to PPARagonists in -irradiated cultures promotes cell survival.
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