Temat: peroxisome proliferator-activated receptor - Katalog OPAC zbiorów

Skocz do pozycji: 1.

Tytuł:: Pioglitazone, a PPAR-gamma ligand, exerts cytostatic/cytotoxic effects against cancer cells, that do not result from inhibition of proteasome
Autorzy:: Mrówka, Piotr
Głodkowska, Eliza
Młynarczuk-Biały, Izabela
Biały, Łukasz
Kuckelkorn, Ulrike
Nowis, Dominika
Makowski, Marcin
Legat, Magdalena
Gołąb, Jakub
Powiązania:: https://bibliotekanauki.pl/articles/1040817.pdf
Data publikacji:: 2008
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: peroxisome proliferator-activated receptor-gamma
thiazolidinediones
proteasome
pioglitazone
Opis:: 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.
Źródło:: Acta Biochimica Polonica; 2008, 55, 1; 75-84
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 2.

Tytuł:: Evidence for differential effects of glucose and cycloheximide on mRNA levels of peroxisome proliferator-activated receptor- (PPAR-) machinery members: Superinduction of PPAR-γ1 and -γ2 mRNAs
Autorzy:: Rypka, Miroslav
Veselý, Jaroslav
Powiązania:: https://bibliotekanauki.pl/articles/1040405.pdf
Data publikacji:: 2010
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: peroxisome proliferator-activated receptor
HepG2 cells
mRNA stability
PPAR-γ coactivator
superinduction
Opis:: 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.
Źródło:: Acta Biochimica Polonica; 2010, 57, 2; 209-215
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 3.

Tytuł:: Ligands of peroxisome proliferator-activated receptor-γ increase the generation of vascular endothelial growth factor in vascular smooth muscle cells and in macrophages.
Autorzy:: Jozkowicz, Alicja
Dulak, Jozef
Piatkowska, Ewa
Placha, Wojciech
Dembinska-Kiec, Aldona
Powiązania:: https://bibliotekanauki.pl/articles/1044268.pdf
Data publikacji:: 2000
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: angiogenesis
ciglitazone
vascular endothelial growth factor
thiazolidinediones
prostaglandin-J2
peroxisome proliferator-activated receptor-γ
Opis:: Peroxisome proliferator-activated receptors-γ (PPARγ) are ligand-inducible transcription factors of the nuclear hormone receptor superfamily. We examined the effect of PPARγ 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 PPARγ activators: prostaglandin J2 and ciglitazone. PPARγ were expressed in VSMC and RAW cells and their activity was upregulated in the presence of PGJ2 and ciglitazone. Incubation of the cells with PPARγ activators significantly augmented the release of VEGF protein into the media, both in resting and in IL-1β- 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 PPARγ upregulates the generation of VEGF and may be involved in the regulation of angiogenesis.
Źródło:: Acta Biochimica Polonica; 2000, 47, 4; 1147-1157
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki

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Skocz do pozycji: 4.

Tytuł:: Prostaglandin-J2 upregulates expression of matrix metalloproteinase-1 independently of activation of peroxisome proliferator-activated receptor-γ.
Autorzy:: Józkowicz, Alicja
Huk, Ihor
Nigisch, Anneliese
Cisowski, Jarosław
Weigel, Guenter
Dulak, Józef
Powiązania:: https://bibliotekanauki.pl/articles/1043441.pdf
Data publikacji:: 2003
Wydawca:: Polskie Towarzystwo Biochemiczne
Tematy:: matrix metalloproteinase-1
urokinase plasminogen activator
prostaglandin-J2
peroxisome proliferator-activated receptor-γ
endothelial cells
Opis:: Peroxisome proliferator-activated receptor-γ (PPARγ) is a ligand-inducible nuclear receptor that functions as a transcription factor involved in lipid metabolism, inflammatory response and angiogenesis. The most potent endogenous PPARγ activator is 15-deoxy-Δ12,14prostaglandin-J2 (15d-PGJ2), whereas synthetic ligands include the oral antidiabetic drugs thiazolidinediones (TZDs). Activation of PPARγ was reported to decrease the synthesis of matrix metalloproteinases (MMPs) in vascular smooth muscle cells and macrophages. We aimed to investigate the effect of PPARγ ligands on expression of MMP-1 and urokinase plasminogen activator (uPA) in human microvascular endothelial cells (HMEC-1). We found that treatment of HMEC-1 with 15d-PGJ2 increased the synthesis of MMP-1 protein up to 168% comparing to untreated cells. TZDs (ciglitazone and troglitazone), more potent activators of PPARγ in HMEC-1, did not influence MMP-1 production, arguing against the involvement of PPARγ in this process. Importantly, the stimulatory effect of 15d-PGJ2 was reversed by the antioxidant N-acetyl-cysteine (NAC), suggesting a contribution of oxidative stress. We demonstrated also that 15d-PGJ2 did not change the activity of MMP-1 promoter, but increased the stability of MMP-1 mRNA. In contrast, 15d-PGJ2 very potently inhibited the synthesis of uPA. This effect was in part mimicked by ciglitazone and troglitazone implying an involvement of PPARγ. Accordingly, NAC did not modify the inhibitory effect of 15d-PGJ2 on uPA expression. In conclusion, we postulate that 15d-PGJ2 may differently regulate the synthesis of proteases involved in angiogenesis : it upregulates MMP-1 expression in HMEC-1 through induction of oxidative stress, and inhibits uPA synthesis partly by activation of PPARγ.
Źródło:: Acta Biochimica Polonica; 2003, 50, 3; 677-689
0001-527X
Pojawia się w:: Acta Biochimica Polonica
Dostawca treści:: Biblioteka Nauki