scholarly journals Identification of the CREB-binding Protein/p300-interacting Protein CITED2 as a Peroxisome Proliferator-activated Receptor α Coregulator

2004 ◽  
Vol 279 (23) ◽  
pp. 24053-24063 ◽  
Author(s):  
Eric S. Tien ◽  
John W. Davis ◽  
John P. Vanden Heuvel
Keyword(s):  
Binding Protein ◽  
Peroxisome Proliferator ◽  
Creb Binding Protein ◽  
Peroxisome Proliferator Activated Receptor ◽  
Interacting Protein

scholarly journals Thioredoxin Binding Protein-2/Thioredoxin-Interacting Protein Is a Critical Regulator of Insulin Secretion and Peroxisome Proliferator-Activated Receptor Function

Endocrinology ◽  
2008 ◽  
Vol 150 (3) ◽  
pp. 1225-1234 ◽  
Author(s):  
Shin-ichi Oka ◽  
Eiji Yoshihara ◽  
Akiko Bizen-Abe ◽  
Wenrui Liu ◽  
Mutsumi Watanabe ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Target Genes ◽  
Binding Protein ◽  
Dynamic Change ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Interacting Protein ◽  
Thioredoxin Interacting Protein ◽  
Nutritional Transition ◽  
Coordinated Regulation

The feeding-fasting nutritional transition triggers a dynamic change in metabolic pathways and is a model for understanding how these pathways are mutually organized. The targeted disruption of the thioredoxin binding protein-2 (TBP-2)/thioredoxin-interacting protein (Txnip)/VDUP1 gene in mice results in lethality with hypertriglyceridemia and hypoglycemia during fasting. To investigate the molecular mechanism of the nutritional transition and the role of TBP-2, microarray analyses were performed using the liver of TBP-2−/− mice in the fed and fasted states. We found that the fasting-induced reduction in the expression of lipogenic genes targeted by insulin (SREBP-1), such as FASN and THRSP, was abolished in TBP-2−/− mice, and the expression of lipoprotein lipase is down-regulated, which was consistent with the lipoprotein profile. TBP-2−/− mice also exhibited enhanced glucose-induced insulin secretion and sensitivity. Another feature of the hepatic gene expression in fed TBP-2−/− mice was the augmented expression of peroxisome proliferator activated receptor (PPAR) target genes, such as CD36, FABP2, ACOT1, and FGF21, to regulate fatty acid consumption. In TBP-2−/− mice, PPARα expression was elevated in the fed state, whereas the fasting-induced up-regulation of PPARα was attenuated. We also detected an increased expression of PPARγ coactivator-1α protein in fed TBP-2−/− mice. TBP-2 overexpression significantly inhibited PPARα-mediated transcriptional activity induced by a specific PPARα ligand in vitro. These results suggest that TBP-2 is a key regulator of PPARα expression and signaling, and coordinated regulation of PPARα and insulin secretion by TBP-2 is crucial in the feeding-fasting nutritional transition. TBP-2/Txnip is a key regulator of PPARα expression and signaling, and coordinated regulation of PPARα and insulin secretion by TBP-2/Txnip is crucial in fasting response.

scholarly journals Peroxisome Proliferator-activated Receptor γ Ligands Suppress the Transcriptional Activation of Cyclooxygenase-2

2001 ◽  
Vol 276 (15) ◽  
pp. 12440-12448 ◽  
Author(s):  
Kotha Subbaramaiah ◽  
Derrick T. Lin ◽  
Janice C. Hart ◽  
Andrew J. Dannenberg
Keyword(s):  
Cyclic Amp ◽  
Promoter Activity ◽  
Binding Protein ◽  
Suppressive Effect ◽  
Peroxisome Proliferator ◽  
Creb Binding Protein ◽  
Response Element ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cyclic Amp Response Element ◽  
Cox 2

We investigated whether peroxisome proliferator-activated receptor γ (PPARγ) ligands (ciglitazone, troglitazone, and 15-deoxy-Δ12,14prostaglandin J2) inhibited cyclooxygenase-2 (COX-2) induction in human epithelial cells. Ligands of PPARγ inhibited phorbol ester (phorbol 12-myristate 13-acetate, PMA)-mediated induction of COX-2 and prostaglandin E2synthesis. Nuclear run-offs revealed increased rates ofCOX-2transcription after treatment with PMA, an effect that was inhibited by PPARγ ligands. PMA-mediated induction ofCOX-2promoter activity was inhibited by PPARγ ligands; this suppressive effect was prevented by overexpressing a dominant negative form of PPARγ or a PPAR response element decoy oligonucleotide. The stimulatory effects of PMA were mediated by a cyclic AMP response element in theCOX-2promoter. Treatment with PMA increased activator protein-1 (AP-1) activity and the binding of c-Jun, c-Fos, and ATF-2 to the cyclic AMP response element, effects that were blocked by PPARγ ligands. These findings raised questions about the mechanism underlying the anti-AP-1 effect of PPARγ ligands. The induction of c-Jun by PMA was blocked by PPARγ ligands. Overexpression of either c-Jun or CREB-binding protein/p300 partially relieved the suppressive effect of PPARγ ligands. When CREB-binding protein and c-Jun were overexpressed together, the ability of PPARγ ligands to suppress PMA-mediated induction ofCOX-2promoter activity was essentially abrogated. Bisphenol A diglycidyl ether, a compound that binds to PPARγ but lacks the ability to activate transcription, also inhibited PMA-mediated induction of AP-1 activity and COX-2. Taken together, these findings are likely to be important for understanding the anti-inflammatory and anti-cancer properties of PPARγ ligands.

PPARδ-mediated p21/p27 induction via increased CREB-binding protein nuclear translocation in beraprost-induced antiproliferation of murine aortic smooth muscle cells

2009 ◽  
Vol 297 (2) ◽  
pp. C321-C329 ◽  
Author(s):  
Yuh-Mou Sue ◽  
Chih-Peng Chung ◽  
Heng Lin ◽  
Ying Chou ◽  
Chih-Yu Jen ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Transcriptional Activation ◽  
Nuclear Translocation ◽  
Binding Protein ◽  
Peroxisome Proliferator ◽  
Creb Binding Protein ◽  
Promoter Regions ◽  
Peroxisome Proliferator Activated Receptor ◽  
Aortic Smooth Muscle ◽  
Responsive Element

We previously showed that an increase in the peroxisome proliferator-activated receptor-δ (PPARδ), together with subsequent induction of inducible nitric oxide synthase (iNOS) by beraprost (BPS), inhibits aortic smooth muscle cell proliferation. Herein, we delineated the mechanisms of the antiproliferative effects of BPS through the induction of p21/p27. BPS concentration dependently induced the p21/p27 promoter- and consensus cAMP-responsive element (CRE)-driven luciferase activities, which were significantly suppressed by blocking PPARδ activation. Surprisingly, other than altering the CRE-binding protein (CREB), BPS-mediated PPARδ activation increased nuclear localization of the CREB-binding protein (CBP), a coactivator, which was further confirmed by chromatin immunoprecipitation. Furthermore, novel functional PPAR-responsive elements (PPREs) next to CREs in the rat p21/p27 promoter regions were identified, where PPARδ interacted with CREB through CBP recruitment. BPS-mediated suppression of restenosis in mice with angioplasty was associated with p21/p27 induction. Herein, we demonstrate for the first time that BPS-mediated PPARδ activation enhances transcriptional activation of p21/p27 by increasing CBP nuclear translocation, which contributes to the vasoprotective action of BPS.

scholarly journals The Impact of Anthocyanins and Iridoids on Transcription Factors Crucial for Lipid and Cholesterol Homeostasis

2021 ◽  
Vol 22 (11) ◽  
pp. 6074
Author(s):  
Maciej Danielewski ◽  
Agnieszka Matuszewska ◽  
Adam Szeląg ◽  
Tomasz Sozański
Keyword(s):  
Transcription Factors ◽  
Cholesterol Metabolism ◽  
Binding Protein ◽  
Regulatory Element ◽  
Cholesterol Homeostasis ◽  
Lipid Lowering ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Cell Functions ◽  
The Impact

Nutrition determines our health, both directly and indirectly. Consumed foods affect the functioning of individual organs as well as entire systems, e.g., the cardiovascular system. There are many different diets, but universal guidelines for proper nutrition are provided in the WHO healthy eating pyramid. According to the latest version, plant products should form the basis of our diet. Many groups of plant compounds with a beneficial effect on human health have been described. Such groups include anthocyanins and iridoids, for which it has been proven that their consumption may lead to, inter alia, antioxidant, cholesterol and lipid-lowering, anti-obesity and anti-diabetic effects. Transcription factors directly affect a number of parameters of cell functions and cellular metabolism. In the context of lipid and cholesterol metabolism, five particularly important transcription factors can be distinguished: liver X receptor (LXR), peroxisome proliferator-activated receptor-α (PPAR-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), CCAAT/enhancer binding protein α (C/EBPα) and sterol regulatory element-binding protein 1c (SREBP-1c). Both anthocyanins and iridoids may alter the expression of these transcription factors. The aim of this review is to collect and systematize knowledge about the impact of anthocyanins and iridoids on transcription factors crucial for lipid and cholesterol homeostasis.

Sign in / Sign up

Export Citation Format

Share Document