Endothelial autophagy is not required for liver regeneration after partial hepatectomy in mice with fatty liver.


Journal

Liver international : official journal of the International Association for the Study of the Liver
ISSN: 1478-3231
Titre abrégé: Liver Int
Pays: United States
ID NLM: 101160857

Informations de publication

Date de publication:
10 2023
Historique:
revised: 18 06 2023
received: 15 10 2022
accepted: 20 06 2023
medline: 19 9 2023
pubmed: 5 7 2023
entrez: 4 7 2023
Statut: ppublish

Résumé

Patients with non-alcoholic fatty liver disease (NAFLD) have impaired liver regeneration. Liver endothelial cells play a key role in liver regeneration. In non-alcoholic steatohepatitis (NASH), liver endothelial cells display a defect in autophagy, contributing to NASH progression. We aimed to determine the role of endothelial autophagy in liver regeneration following liver resection in NAFLD. First, we assessed autophagy in primary endothelial cells from wild type mice fed a high fat diet and subjected to partial hepatectomy. Then, we assessed liver regeneration after partial hepatectomy in mice deficient (Atg5 First, autophagy (LC3II/protein) was strongly increased in liver endothelial cells following hepatectomy. Then, we observed at 40 and 48 h and at 7 days after partial hepatectomy, that Atg5 These results demonstrate that the defect in endothelial autophagy occurring in NASH does not account for the impaired liver regeneration occurring in this setting.

Sections du résumé

BACKGROUND & AIMS
Patients with non-alcoholic fatty liver disease (NAFLD) have impaired liver regeneration. Liver endothelial cells play a key role in liver regeneration. In non-alcoholic steatohepatitis (NASH), liver endothelial cells display a defect in autophagy, contributing to NASH progression. We aimed to determine the role of endothelial autophagy in liver regeneration following liver resection in NAFLD.
METHODS
First, we assessed autophagy in primary endothelial cells from wild type mice fed a high fat diet and subjected to partial hepatectomy. Then, we assessed liver regeneration after partial hepatectomy in mice deficient (Atg5
RESULTS
First, autophagy (LC3II/protein) was strongly increased in liver endothelial cells following hepatectomy. Then, we observed at 40 and 48 h and at 7 days after partial hepatectomy, that Atg5
CONCLUSION
These results demonstrate that the defect in endothelial autophagy occurring in NASH does not account for the impaired liver regeneration occurring in this setting.

Identifiants

pubmed: 37403133
doi: 10.1111/liv.15665
doi:

Substances chimiques

Choline N91BDP6H0X
Methionine AE28F7PNPL

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

2309-2319

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2023 The Authors. Liver International published by John Wiley & Sons Ltd.

Références

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Auteurs

Adel Hammoutene (A)

Université Paris Cité, PARCC, INSERM, Paris, France.
Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.

Marion Tanguy (M)

Université Paris Cité, PARCC, INSERM, Paris, France.
Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.

Mélanie Calmels (M)

Université Paris Cité, PARCC, INSERM, Paris, France.

Riccardo Pravisani (R)

Service de chirurgie hépatobiliaire et pancréatique, Hôpital Beaujon, AP-HP, Clichy, France.

Miguel Albuquerque (M)

Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.
Service d'Anatomie Pathologique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France.

Christophe Casteleyn (C)

Department of Morphology, Imaging, Orthopaedics, Physiotherapy and Nutrition, Ghent University, Ghent, Belgium.

Lotfi Slimani (L)

Laboratory of Orofacial Pathologies, Imaging and Biotherapies URP2496, Université Paris Cité, Montrouge, France.
Plateforme Imageries du Vivant, Faculté de Chirurgie Dentaire, Université Paris Cité, Montrouge, France.

Jeremy Sadoine (J)

Laboratory of Orofacial Pathologies, Imaging and Biotherapies URP2496, Université Paris Cité, Montrouge, France.
Plateforme Imageries du Vivant, Faculté de Chirurgie Dentaire, Université Paris Cité, Montrouge, France.

Chantal M Boulanger (CM)

Université Paris Cité, PARCC, INSERM, Paris, France.

Valérie Paradis (V)

Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.
Service d'Anatomie Pathologique, Hôpital Beaujon, Assistance Publique-Hôpitaux de Paris, Clichy, France.

Hélène Gilgenkrantz (H)

Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.

Pierre-Emmanuel Rautou (PE)

Université Paris Cité, PARCC, INSERM, Paris, France.
Université Paris-Cité, Inserm, Centre de recherche sur l'inflammation, UMR 1149, Paris, France.
Service d'Hépatologie, AP-HP, Hôpital Beaujon, DMU DIGEST, Centre de Référence des Maladies Vasculaires du Foie, FILFOIE, ERN RARE-LIVER, Clichy, France.

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