The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis

Abstract Background and aim Liver regeneration is impaired in end-stage liver disease characterized by advanced fibrosis and cirrhosis, where metabolic reprogramming is considered as a therapeutic target. The shift in glutaminolysis from liver-type Glutaminase 2 (GLS2) to kidney-type Glutaminase 1 (...

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Main Authors: Defu Kong, Qi Zhou, Kang He, Janette Heegsma, Hans Blokzijl, Vincent E de Meijer, Klaas Nico Faber
Format: Article
Language:English
Published: Springer 2025-06-01
Series:Cellular and Molecular Life Sciences
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Online Access:https://doi.org/10.1007/s00018-025-05772-z
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author Defu Kong
Qi Zhou
Kang He
Janette Heegsma
Hans Blokzijl
Vincent E de Meijer
Klaas Nico Faber
author_facet Defu Kong
Qi Zhou
Kang He
Janette Heegsma
Hans Blokzijl
Vincent E de Meijer
Klaas Nico Faber
author_sort Defu Kong
collection DOAJ
description Abstract Background and aim Liver regeneration is impaired in end-stage liver disease characterized by advanced fibrosis and cirrhosis, where metabolic reprogramming is considered as a therapeutic target. The shift in glutaminolysis from liver-type Glutaminase 2 (GLS2) to kidney-type Glutaminase 1 (GLS1) is crucial in different liver diseases, though its role in liver progenitor cell-mediated regeneration remains unclear. This study aimed to analyze the expression of glutamine-metabolizing enzymes in fibrotic human livers and investigate the role of GLS1 in LGR5+-progenitor cell expansion in liver regeneration. Methods Healthy and chronically diseased human liver tissue from patients with alcoholic liver disease, viral hepatitis, biliary atresia, primary biliary cholangitis or non-alcoholic steatohepatitis were immunostained for GLS1, GLS2 and glutamine synthetase (GS), and co-stained for LGR5. GLS1 was inhibited in adult progenitor cell-rived human liver organoids to evaluate its role in stemness and cell proliferation pathways. Results GLS1 expression was enhanced and GLS2 decreased in chronic liver diseases compared to healthy liver. GLS1 was expressed in parenchymal, including hepatocytes, and non-parenchymal cells. In cirrhotic livers, GLS1+ hepatocytes showed a spatial distribution comparable to the progenitor cell marker LGR5. The GLS1 inhibitor CB839 suppressed progenitor cell markers (LGR5 and AXIN2) via the ROS-Wnt/β-Catenin pathway, which was rescued by glutathione (GSH). The CB839-mediated decrease in cell proliferation in human liver organoids was rescued by non-essential amino acids. Conclusions This study identifies GLS1 as a metabolic regulator of progenitor cell expansion aiding liver regeneration in various etiologies of human liver cirrhosis.
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spelling doaj-art-ca51e97779884c8483322e9f5491a3a82025-08-20T03:27:09ZengSpringerCellular and Molecular Life Sciences1420-90712025-06-0182111710.1007/s00018-025-05772-zThe metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosisDefu Kong0Qi Zhou1Kang He2Janette Heegsma3Hans Blokzijl4Vincent E de Meijer5Klaas Nico Faber6Department of Gastroenterology and Hepatology, University of Groningen, University Medical Center GroningenDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center GroningenDepartment of Liver Surgery, Renji Hospital, School of Medicine, Shanghai Jiao Tong UniversityDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center GroningenDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center GroningenDepartment of Surgery, University of Groningen, University Medical Center GroningenDepartment of Gastroenterology and Hepatology, University of Groningen, University Medical Center GroningenAbstract Background and aim Liver regeneration is impaired in end-stage liver disease characterized by advanced fibrosis and cirrhosis, where metabolic reprogramming is considered as a therapeutic target. The shift in glutaminolysis from liver-type Glutaminase 2 (GLS2) to kidney-type Glutaminase 1 (GLS1) is crucial in different liver diseases, though its role in liver progenitor cell-mediated regeneration remains unclear. This study aimed to analyze the expression of glutamine-metabolizing enzymes in fibrotic human livers and investigate the role of GLS1 in LGR5+-progenitor cell expansion in liver regeneration. Methods Healthy and chronically diseased human liver tissue from patients with alcoholic liver disease, viral hepatitis, biliary atresia, primary biliary cholangitis or non-alcoholic steatohepatitis were immunostained for GLS1, GLS2 and glutamine synthetase (GS), and co-stained for LGR5. GLS1 was inhibited in adult progenitor cell-rived human liver organoids to evaluate its role in stemness and cell proliferation pathways. Results GLS1 expression was enhanced and GLS2 decreased in chronic liver diseases compared to healthy liver. GLS1 was expressed in parenchymal, including hepatocytes, and non-parenchymal cells. In cirrhotic livers, GLS1+ hepatocytes showed a spatial distribution comparable to the progenitor cell marker LGR5. The GLS1 inhibitor CB839 suppressed progenitor cell markers (LGR5 and AXIN2) via the ROS-Wnt/β-Catenin pathway, which was rescued by glutathione (GSH). The CB839-mediated decrease in cell proliferation in human liver organoids was rescued by non-essential amino acids. Conclusions This study identifies GLS1 as a metabolic regulator of progenitor cell expansion aiding liver regeneration in various etiologies of human liver cirrhosis.https://doi.org/10.1007/s00018-025-05772-zGlutamine metabolismGlutaminase 1GSHProliferationLiver fibrosisLiver organoids
spellingShingle Defu Kong
Qi Zhou
Kang He
Janette Heegsma
Hans Blokzijl
Vincent E de Meijer
Klaas Nico Faber
The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
Cellular and Molecular Life Sciences
Glutamine metabolism
Glutaminase 1
GSH
Proliferation
Liver fibrosis
Liver organoids
title The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
title_full The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
title_fullStr The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
title_full_unstemmed The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
title_short The metabolic shift of glutaminase 2 to glutaminase 1 promotes LGR5 + progenitor cell proliferation in liver cirrhosis
title_sort metabolic shift of glutaminase 2 to glutaminase 1 promotes lgr5 progenitor cell proliferation in liver cirrhosis
topic Glutamine metabolism
Glutaminase 1
GSH
Proliferation
Liver fibrosis
Liver organoids
url https://doi.org/10.1007/s00018-025-05772-z
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