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101. The Nuclear Hormone Receptor Peroxisome Proliferator-Activated Receptor β/δ Potentiates Cell Chemotactism, Polarization, and Migration.

Author

Nguan Soon Tan, Icre, Guillaume, Montagner, Alexandra, Heggeler, Béatrice Bordier-ten, Wahli, Walter, and Michalik, Liliane

Subjects
HORMONE receptors, PEROXISOMES, KERATINOCYTES, CELL migration, PROTEIN kinases, RHO GTPases, INTEGRINS
Abstract

After an injury, keratinocytes acquire the plasticity necessary for the reepithelialization of the wound. Here, we identify a novel pathway by which a nuclear hormone receptor, until now better known for its metabolic functions, potentiates cell migration. We show that peroxisome proliferator-activated receptor β/δ (PPARβ/δ) enhances two phosphatidylinositol 3-kinase-dependent pathways, namely, the Akt and the Rho-GTPase pathways. This PPARβ/δ activity amplifies the response of keratinocytes to a chemotactic signal, promotes integrin recycling and remodeling of the actin cytoskeleton, and thereby favors cell migration. Using three-dimensional wound reconstructions, we demonstrate that these defects have a strong impact on in vivo skin healing, since PPARβ/δ/ mice show an unexpected and rare epithelialization phenotype. Our findings demonstrate that nuclear hormone receptors not only regulate intercellular communication at the organism level but also participate in cell responses to a chemotactic signal. The implications of our findings may be far-reaching, considering that the mechanisms described here are important in many physiological and pathological situations. [ABSTRACT FROM AUTHOR]

Published
2007
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102. Hepatic fasting-induced PPAR alpha activity does not depend on essential fatty acids

Author

Arnaud Polizzi, Alexandra Montagner, A. Marmugi, Walter Wahli, Laila Mselli-Lakhal, Frédéric Lasserre, Edwin Fouché, Nicolas Loiseau, Simon Ducheix, Hervé Guillou, ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Lee Kong Chian School of Medicine, Nanyang Technological University [Singapour], Center for Integrative Genomics, Université de Lausanne, This work was funded by the Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore Start-Up Grant (to Walter Wahli), by ANRs 'Hepatokind' (to Herve Guillou). Alexandra Montagner, Walter Wahli, and Herve Guillou were supported by Région Midi-Pyrénées, Lee Kong Chian School of Medicine (LKCMedicine), Guillou, Hervé, Montagner, Alexandra, Toxicologie Intégrative & Métabolisme (ToxAlim-TIM), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Prévention et promotion de la cancérogénèse par les aliments (ToxAlim-PPCA), Exposition, Perturbation Endocrino-métabolique et Reproduction (ToxAlim-EXPER), Nanyang Technological University (NTU), Center for Integrative Genomics - Institute of Bioinformatics, Génopode (CIG), Swiss Institute of Bioinformatics [Lausanne] (SIB), and Université de Lausanne (UNIL)-Université de Lausanne (UNIL)

Subjects
Male, 0301 basic medicine, récepteur ppar, liver diseases, Peroxisome proliferator-activated receptor, nuclear receptors, human health, PPARα, lcsh:Chemistry, Mice, chemistry.chemical_compound, 0302 clinical medicine, pparalpha, Cytochrome P-450 Enzyme System, steatosis, nuclear receptor, Receptor, lcsh:QH301-705.5, Spectroscopy, récepteur nucléaire, Mice, Knockout, chemistry.chemical_classification, biology, acide gras, dietary fatty acids, Alanine Transaminase, General Medicine, santé humaine, polyunsaturated fatty acid, Computer Science Applications, Cholesterol, Liver, fasting, polyunsaturated fatty acids, PPAR alpha, 030211 gastroenterology & hepatology, Polyunsaturated fatty acid, medicine.medical_specialty, Médecine humaine et pathologie, Article, Catalysis, Inorganic Chemistry, 03 medical and health sciences, acide gras polyinsaturé, Internal medicine, medicine, Animals, Aspartate Aminotransferases, Cytochrome P450 Family 4, RNA, Messenger, Alanine Transaminase/blood, Aspartate Aminotransferases/blood, Body Weight, Cholesterol/blood, Cytochrome P-450 Enzyme System/genetics, Cytochrome P450 Family 4/genetics, Dietary Fats, Fasting, Fatty Liver/metabolism, Fatty Liver/pathology, Fibroblast Growth Factors/genetics, Liver/metabolism, Liver/pathology, Mice, Inbred C57BL, PPAR alpha/genetics, PPAR alpha/metabolism, RNA, Messenger/metabolism, Triglycerides/blood, Physical and Theoretical Chemistry, adipocyte protein 2, Molecular Biology, Triglycerides, stéatose, Fatty acid metabolism, Organic Chemistry, Fatty acid, medicine.disease, Fatty Liver, Fibroblast Growth Factors, 030104 developmental biology, Endocrinology, lcsh:Biology (General), lcsh:QD1-999, chemistry, biology.protein, Human health and pathology, fatty acid, Steatosis, maladie du foie, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Hormone
Abstract

The liver plays a central role in the regulation of fatty acid metabolism, which is highly sensitive to transcriptional responses to nutrients and hormones. Transcription factors involved in this process include nuclear hormone receptors. One such receptor, PPARα, which is highly expressed in the liver and activated by a variety of fatty acids, is a critical regulator of hepatic fatty acid catabolism during fasting. The present study compared the influence of dietary fatty acids and fasting on hepatic PPARα-dependent responses. Pparα(-/-) male mice and their wild-type controls were fed diets containing different fatty acids for 10 weeks prior to being subjected to fasting or normal feeding. In line with the role of PPARα in sensing dietary fatty acids, changes in chronic dietary fat consumption influenced liver damage during fasting. The changes were particularly marked in mice fed diets lacking essential fatty acids. However, fasting, rather than specific dietary fatty acids, induced acute PPARα activity in the liver. Taken together, the data imply that the potent signalling involved in triggering PPARα activity during fasting does not rely on essential fatty acid-derived ligand. Published version

Published
2016

103. GW501516-activated PPARbeta/delta promotes liver fibrosis via p38-JNK MAPK-induced hepatic stellate cell proliferation

Author

Hervé Guillou, Sébastien Fleury, Walter Wahli, Alexandra Montagner, Erwan Gouranton, David Dombrowicz, Pierre Desreumaux, Radina Kostadinova, Center for Integrative Genomics - Institute of Bioinformatics, Génopode (CIG), Swiss Institute of Bioinformatics [Lausanne] (SIB), Université de Lausanne (UNIL)-Université de Lausanne (UNIL), ToxAlim (ToxAlim), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA), Récepteurs nucléaires, maladies cardiovasculaires et diabète (EGID), Université de Lille, Droit et Santé-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), This work was supported by grants from the Swiss National Science Foundation (WW), the Bonizzi-Theler-Stiftung (WW), the Roche Foundation (WW and AM), the Fondation pour la Recherche Médicale (AM), the 7th EU program TORNADO (WW) and the Etat de Vaud., Université de Lausanne = University of Lausanne (UNIL)-Université de Lausanne = University of Lausanne (UNIL), Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), Université de Toulouse (UT)-Université de Toulouse (UT)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université de Toulouse (UT)-Ecole d'Ingénieurs de Purpan (INP - PURPAN), Université de Toulouse (UT)-Université de Toulouse (UT), Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 (RNMCD), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Toxicologie Intégrative & Métabolisme (ToxAlim-TIM), Université de Toulouse (UT)-Université de Toulouse (UT)-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3), European Project: 222720,EC | FP7 | SP1 | KBBE ,FP7-KBBE-2007-2A,TORNADO(2009), Montagner, Alexandra, Guillou, Hervé, Wahli, Walter, BMC, Ed., Molecular Targets Open for Regulation by the gut flora – New Avenues for improved Diet to Optimize European health - TORNADO - - EC | FP7 | SP1 | KBBE 2009-09-01 - 2014-08-31 - 222720 - VALID, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Ecole d'Ingénieurs de Purpan (INPT - EI Purpan), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Recherche Agronomique (INRA)-Université Toulouse III - Paul Sabatier (UT3)

Subjects
Hepatic stellate cell proliferation, medicine.medical_specialty, Signaling pathways, lcsh:Biotechnology, p38 mitogen-activated protein kinases, Proliferation, Peroxisome proliferator-activated receptor, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, General Biochemistry, Genetics and Molecular Biology, lcsh:Biochemistry, 03 medical and health sciences, 0302 clinical medicine, lcsh:TP248.13-248.65, Internal medicine, medicine, lcsh:QD415-436, Peroxisome proliferator-activated receptor beta/delta, Inflammation, Fibrosis, lcsh:QH301-705.5, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, 030304 developmental biology, Peroxisome proliferator-activated receptor β/δ, chemistry.chemical_classification, Liver injury, 0303 health sciences, Kinase, Research, medicine.disease, 3. Good health, Cell biology, Endocrinology, lcsh:Biology (General), chemistry, 030220 oncology & carcinogenesis, peroxisome proliferator-activated receptor beta/delta, inflammation, fibrosis, signaling pathway, proliferation, Hepatic stellate cell, Signal transduction, Autre (Sciences du Vivant), Transforming growth factor
Abstract

Background After liver injury, the repair process comprises activation and proliferation of hepatic stellate cells (HSCs), which produce extracellular matrix (ECM) proteins. Peroxisome proliferator-activated receptor beta/delta ( PPARβ/δ) is highly expressed in these cells, but its function in liver repair remains incompletely understood. This study investigated whether activation of PPARβ/δ with the ligand GW501516 influenced the fibrotic response to injury from chronic carbon tetrachloride (CCl4) treatment in mice. Wild type and PPARβ/δ-null mice were treated with CCl4 alone or CCl4 co-administered with GW501516. To unveil mechanisms underlying the PPARβ/δ-dependent effects, we analyzed the proliferative response of human LX-2 HSCs to GW501516 in the presence or absence of PPARβ/δ. Results We found that GW501516 treatment enhanced the fibrotic response. Compared to the other experimental groups, CCl4/GW501516-treated wild type mice exhibited increased expression of various profibrotic and pro-inflammatory genes, such as those involved in extracellular matrix deposition and macrophage recruitment. Importantly, compared to healthy liver, hepatic fibrotic tissues from alcoholic patients showed increased expression of several PPAR target genes, including phosphoinositide-dependent kinase-1, transforming growth factor beta-1, and monocyte chemoattractant protein-1. GW501516 stimulated HSC proliferation that caused enhanced fibrotic and inflammatory responses, by increasing the phosphorylation of p38 and c-Jun N-terminal kinases through the phosphoinositide-3 kinase/protein kinase-C alpha/beta mixed lineage kinase-3 pathway. Conclusions This study clarified the mechanism underlying GW501516-dependent promotion of hepatic repair by stimulating proliferation of HSCs via the p38 and JNK MAPK pathways.

Published
2012

104. Endoplasmic reticulum stress controls iron metabolism through TMPRSS6 repression and hepcidin mRNA stabilization by RNA-binding protein HuR.

Author

Belot A, Gourbeyre O, Palin A, Rubio A, Largounez A, Besson-Fournier C, Latour C, Lorgouilloux M, Gallitz I, Montagner A, Polizzi A, Régnier M, Smati S, Zhang AS, Diaz-Munoz MD, Steinbicker AU, Guillou H, Roth MP, Coppin H, and Meynard D

Subjects
Humans, Iron metabolism, Membrane Proteins genetics, Membrane Proteins metabolism, RNA, Messenger genetics, RNA-Binding Proteins, Serine Endopeptidases genetics, Endoplasmic Reticulum Stress genetics, Hepcidins genetics, Hepcidins metabolism
Published
2021
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105. Combined QTL and selective sweep mappings with coding SNP annotation and cis-eQTL analysis revealed PARK2 and JAG2 as new candidate genes for adiposity regulation.

Author

Roux PF, Boitard S, Blum Y, Parks B, Montagner A, Mouisel E, Djari A, Esquerré D, Désert C, Boutin M, Leroux S, Lecerf F, Le Bihan-Duval E, Klopp C, Servin B, Pitel F, Duclos MJ, Guillou H, Lusis AJ, Demeure O, and Lagarrigue S

Subjects
Adipose Tissue, White metabolism, Alleles, Animals, Cell Line, Chickens, Chromosome Mapping, Genome, High-Throughput Nucleotide Sequencing, Jagged-2 Protein, Membrane Proteins metabolism, Mice, Molecular Sequence Annotation, Myosins genetics, Myosins metabolism, Polymorphism, Single Nucleotide, Sequence Analysis, DNA, Adiposity genetics, Membrane Proteins genetics, Quantitative Trait Loci, Ubiquitin-Protein Ligases genetics
Abstract

Very few causal genes have been identified by quantitative trait loci (QTL) mapping because of the large size of QTL, and most of them were identified thanks to functional links already known with the targeted phenotype. Here, we propose to combine selection signature detection, coding SNP annotation, and cis-expression QTL analyses to identify potential causal genes underlying QTL identified in divergent line designs. As a model, we chose experimental chicken lines divergently selected for only one trait, the abdominal fat weight, in which several QTL were previously mapped. Using new haplotype-based statistics exploiting the very high SNP density generated through whole-genome resequencing, we found 129 significant selective sweeps. Most of the QTL colocalized with at least one sweep, which markedly narrowed candidate region size. Some of those sweeps contained only one gene, therefore making them strong positional causal candidates with no presupposed function. We then focused on two of these QTL/sweeps. The absence of nonsynonymous SNPs in their coding regions strongly suggests the existence of causal mutations acting in cis on their expression, confirmed by cis-eQTL identification using either allele-specific expression or genetic mapping analyses. Additional expression analyses of those two genes in the chicken and mice contrasted for adiposity reinforces their link with this phenotype. This study shows for the first time the interest of combining selective sweeps mapping, coding SNP annotation and cis-eQTL analyses for identifying causative genes for a complex trait, in the context of divergent lines selected for this specific trait. Moreover, it highlights two genes, JAG2 and PARK2, as new potential negative and positive key regulators of adiposity in chicken and mice., (Copyright © 2015 Roux et al.)

Published
2015
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106. The nuclear hormone receptor peroxisome proliferator-activated receptor beta/delta potentiates cell chemotactism, polarization, and migration.

Author

Tan NS, Icre G, Montagner A, Bordier-ten-Heggeler B, Wahli W, and Michalik L

Subjects
Actins metabolism, Animals, Cells, Cultured, Enzyme Activation, Epidermal Growth Factor metabolism, Humans, Keratinocytes cytology, Keratinocytes physiology, Mice, Mice, Knockout, PPAR delta genetics, PPAR-beta genetics, Phenotype, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt genetics, Proto-Oncogene Proteins c-akt metabolism, Stress Fibers metabolism, Wound Healing, cdc42 GTP-Binding Protein metabolism, rac1 GTP-Binding Protein metabolism, rho GTP-Binding Proteins metabolism, Cell Movement physiology, Cell Polarity, Chemotaxis physiology, PPAR delta metabolism, PPAR-beta metabolism, Signal Transduction physiology
Abstract

After an injury, keratinocytes acquire the plasticity necessary for the reepithelialization of the wound. Here, we identify a novel pathway by which a nuclear hormone receptor, until now better known for its metabolic functions, potentiates cell migration. We show that peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) enhances two phosphatidylinositol 3-kinase-dependent pathways, namely, the Akt and the Rho-GTPase pathways. This PPARbeta/delta activity amplifies the response of keratinocytes to a chemotactic signal, promotes integrin recycling and remodeling of the actin cytoskeleton, and thereby favors cell migration. Using three-dimensional wound reconstructions, we demonstrate that these defects have a strong impact on in vivo skin healing, since PPARbeta/delta-/- mice show an unexpected and rare epithelialization phenotype. Our findings demonstrate that nuclear hormone receptors not only regulate intercellular communication at the organism level but also participate in cell responses to a chemotactic signal. The implications of our findings may be far-reaching, considering that the mechanisms described here are important in many physiological and pathological situations.

Published
2007
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