Tick-tock hedgehog-mutual crosstalk with liver circadian clock promotes liver steatosis.


Journal

Journal of hepatology
ISSN: 1600-0641
Titre abrégé: J Hepatol
Pays: Netherlands
ID NLM: 8503886

Informations de publication

Date de publication:
06 2019
Historique:
received: 08 06 2018
revised: 20 12 2018
accepted: 16 01 2019
pubmed: 4 2 2019
medline: 2 12 2020
entrez: 4 2 2019
Statut: ppublish

Résumé

The mammalian circadian clock controls various aspects of liver metabolism and integrates nutritional signals. Recently, we described Hedgehog (Hh) signaling as a novel regulator of liver lipid metabolism. Herein, we investigated crosstalk between hepatic Hh signaling and circadian rhythm. Diurnal rhythms of Hh signaling were investigated in liver and hepatocytes from mice with ablation of Smoothened (SAC-KO) and crossbreeds with PER2::LUC reporter mice. By using genome-wide screening, qPCR, immunostaining, ELISA and RNAi experiments in vitro we identified relevant transcriptional regulatory steps. Shotgun lipidomics and metabolic cages were used for analysis of metabolic alterations and behavior. Hh signaling showed diurnal oscillations in liver and hepatocytes in vitro. Correspondingly, the level of Indian Hh, oscillated in serum. Depletion of the clock gene Bmal1 in hepatocytes resulted in significant alterations in the expression of Hh genes. Conversely, SAC-KO mice showed altered expression of clock genes, confirmed by RNAi against Gli1 and Gli3. Genome-wide screening revealed that SAC-KO hepatocytes showed time-dependent alterations in various genes, particularly those associated with lipid metabolism. The clock/hedgehog module further plays a role in rhythmicity of steatosis, and in the response of the liver to a high-fat diet or to differently timed starvation. For the first time, Hh signaling in hepatocytes was found to be time-of-day dependent and to feed back on the circadian clock. Our findings suggest an integrative role of Hh signaling, mediated mainly by GLI factors, in maintaining homeostasis of hepatic lipid metabolism by balancing the circadian clock. The results of our investigation show for the first time that the Hh signaling in hepatocytes is time-of-day dependent, leading to differences not only in transcript levels but also in the amount of Hh ligands in peripheral blood. Conversely, Hh signaling is able to feed back to the circadian clock.

Sections du résumé

BACKGROUND & AIMS
The mammalian circadian clock controls various aspects of liver metabolism and integrates nutritional signals. Recently, we described Hedgehog (Hh) signaling as a novel regulator of liver lipid metabolism. Herein, we investigated crosstalk between hepatic Hh signaling and circadian rhythm.
METHODS
Diurnal rhythms of Hh signaling were investigated in liver and hepatocytes from mice with ablation of Smoothened (SAC-KO) and crossbreeds with PER2::LUC reporter mice. By using genome-wide screening, qPCR, immunostaining, ELISA and RNAi experiments in vitro we identified relevant transcriptional regulatory steps. Shotgun lipidomics and metabolic cages were used for analysis of metabolic alterations and behavior.
RESULTS
Hh signaling showed diurnal oscillations in liver and hepatocytes in vitro. Correspondingly, the level of Indian Hh, oscillated in serum. Depletion of the clock gene Bmal1 in hepatocytes resulted in significant alterations in the expression of Hh genes. Conversely, SAC-KO mice showed altered expression of clock genes, confirmed by RNAi against Gli1 and Gli3. Genome-wide screening revealed that SAC-KO hepatocytes showed time-dependent alterations in various genes, particularly those associated with lipid metabolism. The clock/hedgehog module further plays a role in rhythmicity of steatosis, and in the response of the liver to a high-fat diet or to differently timed starvation.
CONCLUSIONS
For the first time, Hh signaling in hepatocytes was found to be time-of-day dependent and to feed back on the circadian clock. Our findings suggest an integrative role of Hh signaling, mediated mainly by GLI factors, in maintaining homeostasis of hepatic lipid metabolism by balancing the circadian clock.
LAY SUMMARY
The results of our investigation show for the first time that the Hh signaling in hepatocytes is time-of-day dependent, leading to differences not only in transcript levels but also in the amount of Hh ligands in peripheral blood. Conversely, Hh signaling is able to feed back to the circadian clock.

Identifiants

pubmed: 30711403
pii: S0168-8278(19)30065-0
doi: 10.1016/j.jhep.2019.01.022
pii:
doi:

Substances chimiques

Gli1 protein, mouse 0
Gli3 protein, mouse 0
Hedgehog Proteins 0
Nerve Tissue Proteins 0
Smo protein, mouse 0
Smoothened Receptor 0
Zinc Finger Protein GLI1 0
Zinc Finger Protein Gli3 0
ihh protein, mouse 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1192-1202

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

Auteurs

Eugenia Marbach-Breitrück (E)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany; Institute of Biochemistry, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany.

Madlen Matz-Soja (M)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany. Electronic address: madlen.matz@medizin.uni-leipzig.de.

Ute Abraham (U)

Laboratory of Chronobiology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany.

Wolfgang Schmidt-Heck (W)

Leibniz Institute for Natural Product Research and Infection Biology - Hans Knoell Institute, Jena, Germany.

Susanne Sales (S)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Christiane Rennert (C)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany; Department of Hepatobiliary Surgery and Visceral Transplantation, University Hospital, Leipzig University, Leipzig, Germany.

Matthias Kern (M)

IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany.

Susanne Aleithe (S)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany; Clinic and Polyclinic of Neurology, Faculty of Medicine, Leipzig University, Germany.

Luise Spormann (L)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany.

Carlo Thiel (C)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany.

Raffaele Gerlini (R)

Institute of Experimental Genetics (IEG), HDC, Neuherberg, Germany.

Katrin Arnold (K)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany.

Nora Klöting (N)

IFB Adiposity Diseases, University of Leipzig, Leipzig, Germany.

Reinhard Guthke (R)

Leibniz Institute for Natural Product Research and Infection Biology - Hans Knoell Institute, Jena, Germany.

Damjana Rozman (D)

Institute of Biochemistry, Faculty of Medicine, University of Ljubljana, Slovenia.

Raffaele Teperino (R)

Institute of Experimental Genetics (IEG), HDC, Neuherberg, Germany; DZD, German Center for Diabetes Research, Neuherberg, Germany.

Andrej Shevchenko (A)

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.

Achim Kramer (A)

Laboratory of Chronobiology, Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Germany.

Rolf Gebhardt (R)

Rudolf-Schönheimer-Institute of Biochemistry, Faculty of Medicine, Leipzig University, Leipzig, Germany. Electronic address: rgebhardt@medizin.uni-leipzig.de.

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Classifications MeSH