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6. RXRs: Collegial Partners

Author

Gilardi, Federica, Desvergne, Béatrice, Harris, Robin, Series editor, Asson-Batres, Mary Ann, editor, and Rochette-Egly, Cécile, editor

Published
2014
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11. Peroxisome proliferator-activated receptor gamma activation is required for maintenance of innate antimicrobial immunity in the colon

Author

Peyrin-Biroulet, Laurent, Beisner, Julia, Wang, Guoxing, Nuding, Sabine, Oommen, Sajit Thottathil, Kelly, Denise, Parmentier-Decrucq, Erika, Dessein, Rodrigue, Merour, Emilie, Chavatte, Philipe, Grandjean, Teddy, Bressenot, Aude, Desreumaux, Pierre, Colombel, Jean-Frédéric, Desvergne, Béatrice, Stange, Eduard F., Wehkamp, Jan, and Chamaillard, Mathias

Published
2010

15. PPARβ/δ governs Wnt signaling and bone turnover

Author

Scholtysek, Carina, Katzenbeisser, Julia, Fu, He, Uderhardt, Stefan, Ipseiz, Natacha, Stoll, Cornelia, Zaiss, Mario M., Stock, Michael, Donhauser, Laura, Bohm, Christina, Kleyer, Arnd, Hess, Andreas, Engelke, Klaus, David, Jean-Pierre, Djouad, Farida, Tuckermann, Jan Peter, Desvergne, Beatrice, Schett, Georg, and Kronke, Gerhard

Subjects
Cellular signal transduction -- Physiological aspects -- Genetic aspects -- Research, Glucose metabolism -- Physiological aspects -- Genetic aspects -- Research, Cell receptors -- Physiological aspects -- Genetic aspects -- Research, Biological sciences, Health
Abstract

Peroxisome proliferator-activated receptors (PPARs) act as metabolic sensors and central regulators of fat and glucose homeostasis (1). Furthermore, PPARγ has been implicated as major catabolic regulator of bone mass in [...]

Published
2013
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19. Crosstalk between peroxisome proliferator-activated receptor [delta] and VEGF stimulates cancer progression

Author

Wang, Dingzhi, Wang, Haibin, Guo, Yong, Ning, Wei, Katkuri, Sharada, Wahli, Walter, Desvergne, Beatrice, Dey, Sudhansu K., and DuBois, Raymond N.

Subjects
Apoptosis -- Research, Colorectal cancer -- Prevention, Colorectal cancer -- Care and treatment, Colorectal cancer -- Research, Vascular endothelial growth factor -- Research, Science and technology
Abstract

Peroxisome proliferator-activated receptor (PPAR) [delta] is a member of the nuclear hormone receptor superfamily. PPAR[delta] may ameliorate metabolic diseases such as obesity and diabetes. However, PPAR[delta]'s role in colorectal carcinogenesis remains controversial. Here, we present genetic and pharmacologic evidence demonstrating that deletion of PPAR[delta] decreases intestinal adenoma growth in [Apc.sup.Min/+] mice and inhibits tumor-promoting effects of a PPAR[delta] agonist GW501516. More importantly, we found that activation of PPAR[delta] up-regulated VEGF in colon carcinoma cells. VEGF directly promotes colon tumor epithelial cell survival through activation of PI3K-Akt signaling. These results not only highlight concerns about the use of PPAR[delta] agonists for treatment of metabolic disorders in patients who are at high risk for colorectal cancer, but also support the rationale for developing PPAR[delta] antagonists for prevention and/or treatment of cancer. apoptosis | colorectal cancer

Published
2006

21. Peroxisome proliferator-activated receptor [gamma] is required in mature white and brown adipocytes for their survival in the mouse

Author

Imai, Takeshi, Takakuwa, Reiko, Marchand, Sandra, Dentz, Emilie, Bornert, Jean-Marc, Messaddeq, Nadia, Wendling, Olivia, Mark, Manuel, Desvergne, Beatrice, Wahli, Walter, Chambon, Pierre, and Metzger, Daniel

Subjects
Peroxisomes -- Research, Science and technology
Abstract

The peroxisome proliferator-activated receptor [gamma] (PPAR[gamma]) mediates the activity of the insulin-sensitizing thiazolidinediones and plays an important role in adipocyte differentiation and fat accretion. The analysis of PPAR[gamma], functions in mature adipocytes is precluded by lethality of PPAR[[gamma].sup.-/-] fetuses and tetraploid-rescued pups. Therefore we have selectively ablated PPAR[gamma] in adipocytes of adult mice by using the tamoxifen-dependent Cre-E[R.sup.T2] recombination system. We show that mature PPAR[gamma]-null white and brown adipocytes die within a few days and are replaced by newly formed PPAR[gamma]-positive adipocytes, demonstrating that PPAR[gamma], is essential for the in vivo survival of mature adipocytes, in addition to its well established requirement for their differentiation. Our data suggest that potent PPAR[gamma] antagonists could be used to acutely reduce obesity. conditional somatic mutagenesis | tamoxifen-dependent | adipocyte maintenance | obesity | nuclear receptor

Published
2004

22. Critical roles of PPAR(beta)/(delta) in keratinocyte response to inflammation

Author

Tan, Nguan Soon, Michalik, Liliane, Noy, Noa, Yasmin, Rubina, Pacot, Corinne, Heim, Manuel, Fluhmann, Beat, Desvergne, Beatrice, and Wahli, Walter

Subjects
Cytochemistry -- Research, Inflammation -- Physiological aspects, Cell death -- Genetic aspects, Cell differentiation -- Research, Keratinocytes -- Research, Biological sciences
Abstract

Roles of PPAR(beta)/(delta) in keratinocyte inflammation response are discussed. Immediately after skin injury comes release of inflammatory signals. Using cultures of primary keratinocytes from wild-type and PPAR(beta)/(delta)(super.-/-) mice has been helpful in finding that such signals induce keratinocyte differentiation through influencing TNF-alpha and IFN-gamma.

Published
2001

23. Roles of PPARs in health and disease

Author

Kersten, Sander, Desvergne, Beatrice, and Wahli, Walter

Subjects
Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Author(s): Sander Kersten; Béatrice Desvergne; Walter Wahli (corresponding author) The PPARs were first cloned as the nuclear receptors that mediate the effects of synthetic compounds called peroxisome proliferators on gene [...]

Published
2000
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26. High risk for hyperlipidemia and the metabolic syndrome after an episode of hypertriglyceridemia during 13-cis retinoic acid therapy for acne: a pharmacogenetic study

Author

Rodondi, Nicolas, Darioli, Roger, Ramelet, Albert-Adrien, Hohl, Daniel, Lenain, Vincent, Perdrix, Jean, Wietlisbach, Vincent, Riesen, Walter F., Walther, Thomas, Medinger, Laurent, Nicod, Pascal, Desvergne, Beatrice, and Mooser, Vincent

Subjects
Acne -- Drug therapy, Isotretinoin -- Adverse and side effects, Lipid metabolism, Health, Accutane (Medication) -- Adverse and side effects
Abstract

Background: Administration of 13-cis retinoic acid (isotretinoin) for acne is occasionally accompanied by hyperlipidemia. It is not known why some persons develop this side effect. Objective: To determine whether isotretinoin triggers a familial susceptibility to hyperlipidemia and the metabolic syndrome. Design: Cross-sectional comparison. Setting: University hospital in Lausanne, Switzerland. Participants: 102 persons in whom triglyceride levels increased at least 1.0 mmol/L (>=89 mg/dL) (hyperresponders) and 100 persons in whom triglyceride levels changed 0.1 mmol/L ( Measurements: Waist-to-hip ratio; fasting glucose, insulin, and lipid levels; and apoE genotype. Results: Hyperresponders and nonresponders had similar pretreatment body weight and plasma lipid levels. When reevaluated approximately 4 years after completion of isotretinoin therapy, hyperresponders were more likely to have hypertriglyceridemia (triglyceride level >2.0 mmol/L [177 mg/dL]; odds ratio [OR], 4.8 [95% CI, 1.6 to 13.8]), hypercholesterolemia (cholesterol level >6.5 mmol/L [>252 mg/dL]; OR, 9.1 [CI, 1.9 to 43]), truncal obesity (waist-to-hip ratio >0.90 [OR, 11.0 (CI, 2.0 to 59]), and hyperinsulinemia (insulin-glucose ratio >7.2; OR, 3.0 [CI, 1.6 to 5.7]). In addition, more hyperrespondes had at least one parent with hypertriglyceridemia (OR, 2.6 [CI, 1.2 to 5.7]) or a ratio of total to high-density lipoprotein cholesterol that exceeded 4.0 (OR, 3.5 [CI, 1.5 to 8.0]). Lipid response to isotretinoin was closely associated with the apoE gene. Conclusion: Persons who develop hypertriglyceridemia during isotretinoin therapy for acne, as well as their parents, are at increased risk for future hyperlipidemia and the metabolic syndrome.

Published
2002

28. Retinaldehyde: more than meets the eye

Author

Desvergne, Beatrice

Abstract

Author(s): Beatrice Desvergne [1] The identification of nuclear receptors defined a new paradigm: small lipophilic hormones specifically bind their cognate receptor and the complex directly regulates the expression of multiple [...]

Published
2007
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30. PPARγ controls pregnancy outcome through activation of EG-VEGF: new insights into the mechanism of placental development

Author

Garnier, Vanessa, primary, Traboulsi, Wael, additional, Salomon, Aude, additional, Brouillet, Sophie, additional, Fournier, Thierry, additional, Winkler, Carine, additional, Desvergne, Beatrice, additional, Hoffmann, Pascale, additional, Zhou, Qun-Yong, additional, Congiu, Cenzo, additional, Onnis, Valentina, additional, Benharouga, Mohamed, additional, Feige, Jean-Jacques, additional, and Alfaidy, Nadia, additional

Published
2015
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31. NCoR1 is a conserved physiological modulator of muscle mass and oxidative function.

Author

Yamamoto, Hiroyasu, Williams, Evan, Mouchiroud, Laurent, Canto, Carles, Fan, Weiwei, Downes, Michael, Heligon, Christophe, Barish, Grant D., Desvergne, Beatrice, Evans, Ronald M., Schoonjans, Kristina, Auwerx, Johan, Yamamoto, Hiroyasu, Williams, Evan, Mouchiroud, Laurent, Canto, Carles, Fan, Weiwei, Downes, Michael, Heligon, Christophe, Barish, Grant D., Desvergne, Beatrice, Evans, Ronald M., Schoonjans, Kristina, and Auwerx, Johan

Abstract

Transcriptional coregulators control the activity of many transcription factors and are thought to have wide-ranging effects on gene expression patterns. We show here that muscle-specific loss of nuclear receptor corepressor 1 (NCoR1) in mice leads to enhanced exercise endurance due to an increase of both muscle mass and of mitochondrial number and activity. The activation of selected transcription factors that control muscle function, such as MEF2, PPARbeta/delta, and ERRs, underpins these phenotypic alterations. NCoR1 levels are decreased in conditions that require fat oxidation, resetting transcriptional programs to boost oxidative metabolism. Knockdown of gei-8, the sole C. elegans NCoR homolog, also robustly increased muscle mitochondria and respiration, suggesting conservation of NCoR1 function. Collectively, our data suggest that NCoR1 plays an adaptive role in muscle physiology and that interference with NCoR1 action could be used to improve muscle function.

Published
2011
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32. mRNA profiling reveals divergent roles of PPARa and PPARß/d in regulating mouse liver gene expression (PPARa samples)

Author

Sanderson-Kjellberg, L.M., Boekschoten, Mark, Desvergne, Beatrice, Muller, Michael, Kersten, Sander, Sanderson-Kjellberg, L.M., Boekschoten, Mark, Desvergne, Beatrice, Muller, Michael, and Kersten, Sander

Abstract

Little is known about the role of the transcription factor PPARß/d in liver. Here we set out to better elucidate the function of PPARß/d in liver by comparing the effect of PPARa and PPARß/d deletion using whole genome transcriptional profiling and analysis of plasma and liver metabolites. In fed state, the number of genes altered by PPARa and PPARß/d deletion was similar, whereas in fasted state the effect of PPARa deletion was much more pronounced, consistent with the pattern of gene expression of PPARa and PPARß/d. Minor overlap was found between PPARa- and PPARß/d-dependent gene regulation in liver. Pathways upregulated by PPARß/d deletion were connected to innate immunity. Pathways downregulated by PPARß/d deletion included lipoprotein metabolism and various pathways related to glucose utilization, which correlated with elevated plasma glucose and triglycerides and reduced plasma cholesterol in PPARß/d-/- mice. Downregulated genes that may underlie these metabolic alterations included Pklr, Fbp1, Apoa4, Vldlr, Lipg, and Pcsk9, which may represent novel PPARß/d target genes. In contrast to PPARa-/- mice, no changes in plasma FFA, plasma ß-hydroxybutyrate, liver triglycerides and liver glycogen were observed in PPARß/d-/- mice. Our data indicate a role for PPARß/d in hepatic glucose utilization and lipoprotein metabolism but not in the adaptive response to fasting., Little is known about the role of the transcription factor PPARß/d in liver. Here we set out to better elucidate the function of PPARß/d in liver by comparing the effect of PPARa and PPARß/d deletion using whole genome transcriptional profiling and analysis of plasma and liver metabolites. In fed state, the number of genes altered by PPARa and PPARß/d deletion was similar, whereas in fasted state the effect of PPARa deletion was much more pronounced, consistent with the pattern of gene expression of PPARa and PPARß/d. Minor overlap was found between PPARa- and PPARß/d-dependent gene regulation in liver. Pathways upregulated by PPARß/d deletion were connected to innate immunity. Pathways downregulated by PPARß/d deletion included lipoprotein metabolism and various pathways related to glucose utilization, which correlated with elevated plasma glucose and triglycerides and reduced plasma cholesterol in PPARß/d-/- mice. Downregulated genes that may underlie these metabolic alterations included Pklr, Fbp1, Apoa4, Vldlr, Lipg, and Pcsk9, which may represent novel PPARß/d target genes. In contrast to PPARa-/- mice, no changes in plasma FFA, plasma ß-hydroxybutyrate, liver triglycerides and liver glycogen were observed in PPARß/d-/- mice. Our data indicate a role for PPARß/d in hepatic glucose utilization and lipoprotein metabolism but not in the adaptive response to fasting.

Published
2009

34. Effect PPARb/d knockout in white adipose tissue

Author

Mandard, S.J., Wahli, Walter, Muller, Michael, Desvergne, Beatrice, Kersten, Sander, Mandard, S.J., Wahli, Walter, Muller, Michael, Desvergne, Beatrice, and Kersten, Sander

Abstract

Analysis of white adipose tissue of PPARb/d knockout mice. Data may point towards putative target genes of PPARb/d and thus the function of PPARb/d in white adipose tissue. Datasets were used to identify glycogen synthase 2 as novel PPAR target., Analysis of white adipose tissue of PPARb/d knockout mice. Data may point towards putative target genes of PPARb/d and thus the function of PPARb/d in white adipose tissue. Datasets were used to identify glycogen synthase 2 as novel PPAR target.

Published
2007

45. Attenuation of Colon Inflammation through Activators of the Retinoid X Receptor (Rxr)/Peroxisome Proliferator–Activated Receptor γ (Pparγ) Heterodimer

Author

Desreumaux, Pierre, primary, Dubuquoy, Laurent, additional, Nutten, Sophie, additional, Peuchmaur, Michel, additional, Englaro, Walter, additional, Schoonjans, Kristina, additional, Derijard, Benoit, additional, Desvergne, Beatrice, additional, Wahli, Walter, additional, Chambon, Pierre, additional, Leibowitz, Mark D., additional, Colombel, Jean-Frédéric, additional, and Auwerx, Johan, additional

Published
2001
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46. Crosstalk between peroxisome proliferator-activated receptor δ and VEGF stimulates cancer progression.

Author

Dingzhi Wang, Wang, Haibin, Yong Guo, Wei Ning, Katkuri, Sharada, Wahli, Walter, Desvergne, Beatrice, Dey, Sudhansu K., and Dubois, Raymond N.

Subjects
PEROXISOMES, VASCULAR endothelial growth factors, TUMOR growth, METABOLIC disorders, HORMONE receptors, ADENOMA
Abstract

Peroxisome proliferator-activated receptor (PPAR) δ is a member of the nuclear hormone receptor superfamily. PPARδ may ameliorate metabolic diseases such as obesity and diabetes. However, PPARδ's role in colorectal carcinogenesis remains controversial. Here, we present genetic and pharmacologic evidence demonstrating that deletion of PPAR6 decreases intestinal adenoma growth in ApcMin/+ mice and inhibits tumor-promoting effects of a PPARδ agonist GW501516. More importantly, we found that activation of PPAR& up-regulated VEGF in colon carcinoma cells. VEGF directly promotes colon tumor epithelial cell survival through activation of PI3K-Akt signaling. These results not only highlight concerns about the use of PPAR6 agonists for treatment of metabolic disorders in patients who are at high risk for colorectat cancer, but also support the rationale for developing PPARδ antagonists for prevention and/or treatment of cancer. [ABSTRACT FROM AUTHOR]

Published
2006
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47. PEROXISOME-PROLIFERATOR-ACTIVATED RECEPTORS AND CANCERS: COMPLEX STORIES.

Author

Michalik, Liliane, Desvergne, Beatrice, and Wahli, Walter

Subjects
*PEROXISOMES, *CANCER, *HORMONE receptors, *FATTY acids, *CELL proliferation, *CARCINOGENESIS
Abstract

Studies the peroxisome-proliferator-activated receptors (PPAR) and cancers. Functions of PPAR, nuclear hormone receptors that mediate the effects of fatty acid and their derivatives; Regulation of cell proliferation, differential and survival; Controlling carcinogenesis in various tissues; Links between each PPAR isotype and carcinogenesis.

Published
2004
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49. PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS: A Nuclear Receptor Signaling Pathway in Lipid Physiology.

Author

Lemberger, Thomas, Desvergne, Beatrice, and Wahli, Walter

Subjects
*PEROXISOMES, *LIPIDS, *TRANSCRIPTION factors, *GENES, *HOMEOSTASIS
Abstract

Peroxisome proliferator-activated receptors (PPARs) are lipid-activated transcription factors that belong to the steroid/thyroid/retinoic acid receptor superfamily. All their characterized target genes encode proteins that participate in lipid homeostasis. The recent finding that antidiabetic thiazolidinediones and adipogenic prostanoids are ligands of one of the PPARs reveals a novel signaling pathway that directly links these compounds to processes involved in glucose homeostasis and lipid metabolism including adipocyte differentiation. A detailed understanding of this pathway could designate PPARs as targets for the development of novel efficient treatments for several metabolic disorders. [ABSTRACT FROM AUTHOR]

Published
1996
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50. Differential regulation of RNA polymerase III genes during liver regeneration

Author

Yeganeh, Meghdad, Praz, Viviane, Carmeli, Cristian, Villeneuve, Dominic, Rib, Leonor, Guex, Nicolas, Herr, Winship, Delorenzi, Mauro, Hernandez, Nouria, Deplancke, Bart, Desvergne, Beatrice, Naef, Felix, Rougemont, Jacques, Schibler, Ueli, Andersin, Teemu, Cousin, Pascal, Gilardi, Federica, Gos, Pascal, Lammers, Fabienne, Lopes, Maykel, Mange, Francois, Minocha, Shilpi, Raghav, Sunil, Fabbretti, Roberto, Vlegel, Volker, Xenarios, Ioannis, Migliavacca, Eugenia, David, Fabrice, Jarosz, Yohan, Kuznetsov, Dmitry, Liechti, Robin, Martin, Olivier, Delafontaine, Julien, Cajan, Julia, Gustafson, Kyle, Krier, Irina, Leleu, Marion, Molina, Nacho, Naldi, Aurelien, Sobel, Jonathan, Symul, Laura, Bounova, Gergana, and Jacquet, Philippe

Subjects
viruses, proliferation, expression, cancer, transcription, pol ii
Abstract

Mouse liver regeneration after partial hepatectomy involves cells in the remaining tissue synchronously entering the cell division cycle. We have used this system and H3K4me3, Pol II and Pol III profiling to characterize adaptations in Pol III transcription. Our results broadly define a class of genes close to H3K4me3 and Pol II peaks, whose Pol III occupancy is high and stable, and another class, distant from Pol II peaks, whose Pol III occupancy strongly increases after partial hepatectomy. Pol III regulation in the liver thus entails both highly expressed housekeeping genes and genes whose expression can adapt to increased demand.

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