Hepatocyte-specific loss of GPS2 in mice ...
Type de document :
Compte-rendu et recension critique d'ouvrage
PMID :
Titre :
Hepatocyte-specific loss of GPS2 in mice reduces non-alcoholic steatohepatitis via activation of PPARα
Auteur(s) :
Liang, Ning [Auteur]
Damdimopoulos, Anastasius [Auteur]
Goñi, Saioa [Auteur]
Huang, Zhiqiang [Auteur]
Vedin, Lise-Lotte [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Jakobsson, Tomas [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Giudici, Marco [Auteur]
Ahmed, Osman [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Pedrelli, Matteo [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Barilla, Serena [Auteur]
Alzaid, Fawaz [Auteur]
Centre de Recherche des Cordeliers [CRC (UMR_S_1138 / U1138)]
Mendoza, Arturo [Auteur]
Weill Medical College of Cornell University [New York]
Schröder, Tarja [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Kuiper, Raoul [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Parini, Paolo [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Hollenberg, Anthony [Auteur]
Weill Medical College of Cornell University [New York]
Lefebvre, Philippe [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Francque, Sven [Auteur]
van Gaal, Luc [Auteur]
Staels, Bart [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Venteclef, Nicolas [Auteur]
Centre de Recherche des Cordeliers [CRC (UMR_S_1138 / U1138)]
Treuter, Eckardt [Auteur correspondant]
Fan, Rongrong [Auteur correspondant]
Damdimopoulos, Anastasius [Auteur]
Goñi, Saioa [Auteur]
Huang, Zhiqiang [Auteur]
Vedin, Lise-Lotte [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Jakobsson, Tomas [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Giudici, Marco [Auteur]
Ahmed, Osman [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Pedrelli, Matteo [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Barilla, Serena [Auteur]
Alzaid, Fawaz [Auteur]
Centre de Recherche des Cordeliers [CRC (UMR_S_1138 / U1138)]
Mendoza, Arturo [Auteur]
Weill Medical College of Cornell University [New York]
Schröder, Tarja [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Kuiper, Raoul [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Parini, Paolo [Auteur]
Department of Laboratory Medicine [Karolinska Institutet]
Hollenberg, Anthony [Auteur]
Weill Medical College of Cornell University [New York]
Lefebvre, Philippe [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Francque, Sven [Auteur]
van Gaal, Luc [Auteur]
Staels, Bart [Auteur]
Récepteurs nucléaires, maladies cardiovasculaires et diabète - U 1011 [RNMCD]
Venteclef, Nicolas [Auteur]
Centre de Recherche des Cordeliers [CRC (UMR_S_1138 / U1138)]
Treuter, Eckardt [Auteur correspondant]
Fan, Rongrong [Auteur correspondant]
Titre de la revue :
Nature Communications
Pagination :
1684
Éditeur :
Nature Publishing Group
Date de publication :
2019-04-11
ISSN :
2041-1723
Discipline(s) HAL :
Sciences du Vivant [q-bio]
Résumé en anglais : [en]
Obesity triggers the development of non-alcoholic fatty liver disease (NAFLD), which involves alterations of regulatory transcription networks and epigenomes in hepatocytes. Here we demonstrate that G protein pathway ...
Lire la suite >Obesity triggers the development of non-alcoholic fatty liver disease (NAFLD), which involves alterations of regulatory transcription networks and epigenomes in hepatocytes. Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR) and histone deacetylase 3 (HDAC3) complex, has a central role in these alterations and accelerates the progression of NAFLD towards non-alcoholic steatohepatitis (NASH). Hepatocyte-specific Gps2 knockout in mice alleviates the development of diet-induced steatosis and fibrosis and causes activation of lipid catabolic genes. Integrative cistrome, epigenome and transcriptome analysis identifies the lipid-sensing peroxisome proliferator-activated receptor α (PPARα, NR1C1) as a direct GPS2 target. Liver gene expression data from human patients reveal that Gps2 expression positively correlates with a NASH/fibrosis gene signature. Collectively, our data suggest that the GPS2-PPARα partnership in hepatocytes coordinates the progression of NAFLD in mice and in humans and thus might be of therapeutic interest.Lire moins >
Lire la suite >Obesity triggers the development of non-alcoholic fatty liver disease (NAFLD), which involves alterations of regulatory transcription networks and epigenomes in hepatocytes. Here we demonstrate that G protein pathway suppressor 2 (GPS2), a subunit of the nuclear receptor corepressor (NCOR) and histone deacetylase 3 (HDAC3) complex, has a central role in these alterations and accelerates the progression of NAFLD towards non-alcoholic steatohepatitis (NASH). Hepatocyte-specific Gps2 knockout in mice alleviates the development of diet-induced steatosis and fibrosis and causes activation of lipid catabolic genes. Integrative cistrome, epigenome and transcriptome analysis identifies the lipid-sensing peroxisome proliferator-activated receptor α (PPARα, NR1C1) as a direct GPS2 target. Liver gene expression data from human patients reveal that Gps2 expression positively correlates with a NASH/fibrosis gene signature. Collectively, our data suggest that the GPS2-PPARα partnership in hepatocytes coordinates the progression of NAFLD in mice and in humans and thus might be of therapeutic interest.Lire moins >
Langue :
Anglais
Vulgarisation :
Non
Projet ANR :
Source :
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- https://www.hal.inserm.fr/inserm-02154801/document
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- https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6459876/pdf
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- Liang%20Nat%20Commun.pdf
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