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Article ; Online: Targeting bile salt homeostasis in biliary diseases.

Trampert, David C / Kunst, Roni F / van de Graaf, Stan F J

2024 Volume 40, Issue 2, Page(s) 62–69

Abstract: Purpose of review: Advances in the understanding of bile salt synthesis, transport and signalling show the potential of modulating bile salt homeostasis as a therapeutic strategy in cholestatic liver diseases. Here, recent developments in (pre)clinical ... ...

Abstract	Purpose of review: Advances in the understanding of bile salt synthesis, transport and signalling show the potential of modulating bile salt homeostasis as a therapeutic strategy in cholestatic liver diseases. Here, recent developments in (pre)clinical research in this field is summarized and discussed. Recent findings: Inhibition of the apical sodium-dependent bile salt transporter (ASBT) and Na + -taurocholate cotransporting polypeptide (NTCP) seems effective against cholestatic liver diseases, as well as Farnesoid X receptor (FXR) agonism or a combination of both. While approved for the treatment of primary biliary cholangitis (PBC) and intrahepatic cholestasis of pregnancy (ICP), ursodeoxycholic acid (UDCA) has retrospectively shown carefully promising results in primary sclerosing cholangitis (PSC). The side chain shortened derivate norUDCA is of further therapeutic interest since its mechanisms of action are independent of the bile salt transport machinery. In the pathogenesis of sclerosing cholangiopathies, a skewed T-cell response with alterations in gut microbiota and bile salt pool compositions are observed. In PSC pathogenesis, the bile salt receptor Takeda G-protein-coupled receptor 5 (TGR5) in cholangiocytes is implicated, whilst in immunoglobulin G4-related cholangitis the autoantigens annexin A11 and laminin 511-E8 are involved in protecting cholangiocytes. Summary: Modulating bile salt homeostasis has proven a promising treatment strategy in models of cholestasis and are continuously being further developed. Confirmatory clinical studies are needed in order to assess the proposed treatment strategies in patients allowing for a broader therapeutic arsenal in the future.
MeSH term(s)	Humans ; Bile Acids and Salts ; Retrospective Studies ; Ursodeoxycholic Acid/therapeutic use ; Cholestasis/drug therapy ; Cholestasis, Intrahepatic/drug therapy ; Homeostasis
Chemical Substances	Bile Acids and Salts ; Ursodeoxycholic Acid (724L30Y2QR)
Language	English
Publishing date	2024-01-10
Publishing country	United States
Document type	Review ; Journal Article
ZDB-ID	632571-3
ISSN	1531-7056 ; 0267-1379
ISSN (online)	1531-7056
ISSN	0267-1379
DOI	10.1097/MOG.0000000000000997
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Zs.A 2072: Show issues

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Article ; Online: Bile Salts by the Back Road.

Oude Elferink, Ronald P J / Van De Graaf, Stan F J

Cellular and molecular gastroenterology and hepatology

2023 Volume 16, Issue 2, Page(s) 319–320

MeSH term(s)	Bile Acids and Salts/metabolism ; Liver/metabolism ; Enterohepatic Circulation
Chemical Substances	Bile Acids and Salts
Language	English
Publishing date	2023-05-24
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	2819778-1
ISSN	2352-345X ; 2352-345X
ISSN (online)	2352-345X
ISSN	2352-345X
DOI	10.1016/j.jcmgh.2023.05.005
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Article ; Online: Bile salt signaling and bile salt-based therapies in cardiometabolic disease.

Groenen, Claire C J / Nguyen, Thuc-Anh / Paulusma, Coen C / van de Graaf, Stan F J

Clinical science (London, England : 1979)

2024 Volume 138, Issue 1, Page(s) 1–21

Abstract: Bile salts have an established role in the emulsification and intestinal absorption of dietary lipids, and their homeostasis is tightly controlled by various transporters and regulators in the enterohepatic circulation. Notably, emerging evidence points ... ...

Abstract	Bile salts have an established role in the emulsification and intestinal absorption of dietary lipids, and their homeostasis is tightly controlled by various transporters and regulators in the enterohepatic circulation. Notably, emerging evidence points toward bile salts as major modulators of cardiometabolic disease (CMD), an umbrella disease of disorders affecting the heart and blood vessels that is caused by systemic metabolic diseases such as Type 2 diabetes mellitus (T2DM) and metabolic dysfunction-associated steatotic liver disease (MASLD), the latter encompassing also metabolic dysfunction-associated steatohepatitis (MASH). The underlying mechanisms of protective effects of bile salts are their hormonal properties, enabling them to exert versatile metabolic effects by activating various bile salt-responsive signaling receptors with the nuclear farnesoid X receptor (FXR) and the Takeda G-protein-coupled receptor 5 (TGR5) as most extensively investigated. Activation of FXR and TGR5 is involved in the regulation of glucose, lipid and energy metabolism, and inflammation. Bile salt-based therapies directly targeting FXR and TGR5 signaling have been evaluated for their therapeutic potential in CMD. More recently, therapeutics targeting bile salt transporters thereby modulating bile salt localization, dynamics, and signaling, have been developed and evaluated in CMD. Here, we discuss the current knowledge on the contribution of bile salt signaling in the pathogenesis of CMD and the potential of bile salt-based therapies for the treatment of CMD.
MeSH term(s)	Humans ; Diabetes Mellitus, Type 2/drug therapy ; Signal Transduction ; Bile Acids and Salts ; Energy Metabolism ; Fatty Liver ; Membrane Transport Proteins ; Cardiovascular Diseases/drug therapy
Chemical Substances	Bile Acids and Salts ; Membrane Transport Proteins
Language	English
Publishing date	2024-01-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	206835-7
ISSN	1470-8736 ; 0301-0538 ; 0009-0360 ; 0143-5221
ISSN (online)	1470-8736
ISSN	0301-0538 ; 0009-0360 ; 0143-5221
DOI	10.1042/CS20230934
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Article ; Online: Insufficient evidence for NTCP activity in stellate cells.

Kunst, Roni F / Paulusma, Coen C / van de Graaf, Stan F J

Gut

2021

Language	English
Publishing date	2021-12-15
Publishing country	England
Document type	Letter
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2021-326452
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Zs.A 160: Show issues

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Article ; Online: Galectin-3 and prohibitin 1 are autoantigens in IgG4-related cholangitis without clear-cut protective effects against toxic bile acids.

Kersten, Remco / Trampert, David C / Hubers, Lowiek M / Tolenaars, Dagmar / Vos, Harmjan R / van de Graaf, Stan F J / Beuers, Ulrich

Frontiers in immunology

2024 Volume 14, Page(s) 1251134

Abstract: Background and aims: IgG4-related cholangitis (IRC) is the hepatobiliary manifestation of IgG4-related disease, a systemic B cell-driven fibro-inflammatory disorder. Four autoantigens have recently been described in IgG4-RD: annexin A11, galectin-3, ... ...

Abstract	Background and aims: IgG4-related cholangitis (IRC) is the hepatobiliary manifestation of IgG4-related disease, a systemic B cell-driven fibro-inflammatory disorder. Four autoantigens have recently been described in IgG4-RD: annexin A11, galectin-3, laminin 511-E8, and prohibitin 1. We have previously reported a protective role of annexin A11 and laminin 511-E8 in human cholangiocytes against toxic bile acids. Here, we explored the potentially protective role of the carbohydrate-binding lectin galectin-3 and the scaffold proteins prohibitins 1 and 2. Methods: Anti-galectin-3, anti-prohibitin 1 and 2 autoantibody positivity in IRC and healthy and disease (primary sclerosing cholangitis (PSC)) control sera was assessed by ELISA/liquid chromatography-tandem mass spectrometry (LC-MS/MS). Human H69 cholangiocytes were subjected to short hairpin RNA (shRNA) knockdown targeting galectin-3 ( Results: Anti-galectin-3 autoantibodies were detected in 13.5% of individuals with IRC but not in PSC. Knockdown of Conclusions: A subset of individuals with IRC have autoantibodies against galectin-3 and prohibitin 1. Gene-specific knockdown, pharmacological inhibition, and recombinant protein substitution did not clearly disclose a protective role of these autoantigens in human cholangiocytes against toxic bile acids. The involvement of these autoantibodies in processes surpassing epithelial secretion remains to be elucidated.
MeSH term(s)	Humans ; Annexins ; Autoantibodies ; Autoantigens ; Bile Acids and Salts ; Cholangitis/immunology ; Chromatography, Liquid ; Galectin 3/immunology ; Immunoglobulin G ; Immunoglobulin G4-Related Disease ; Prohibitins/immunology ; Tandem Mass Spectrometry
Chemical Substances	Annexins ; Autoantibodies ; Autoantigens ; Bile Acids and Salts ; Galectin 3 ; Immunoglobulin G ; Prohibitins ; PHB protein, human
Language	English
Publishing date	2024-01-25
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2023.1251134
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Article ; Online: Laminin 511-E8, an autoantigen in IgG4-related cholangitis, contributes to cholangiocyte protection.

Trampert, David C / Kersten, Remco / Tolenaars, Dagmar / Jongejan, Aldo / van de Graaf, Stan F J / Beuers, Ulrich

JHEP reports : innovation in hepatology

2024 Volume 6, Issue 4, Page(s) 101015

Abstract: Background & aims: IgG4-related cholangitis (IRC) is the hepatobiliary manifestation of IgG4-related disease. Anti-laminin 511-E8 autoantibodies have been identified in its pancreatic manifestation. Laminin 511-E8 promotes endothelial barrier function, ... ...

Abstract	Background & aims: IgG4-related cholangitis (IRC) is the hepatobiliary manifestation of IgG4-related disease. Anti-laminin 511-E8 autoantibodies have been identified in its pancreatic manifestation. Laminin 511-E8 promotes endothelial barrier function, lymphocyte recruitment, and cholangiocyte differentiation. Here, we investigate anti-laminin 511-E8 autoantibody presence in IRC, and mechanisms via which laminin 511 may contribute to cholangiocyte protection. Methods: Anti-laminin 511-E8 serum autoantibody positivity was assessed by ELISA. RNA sequencing and RT-qPCR were performed on human H69 cholangiocytes treated with recombinant laminin 511-E8. H69 cholangiocytes were subjected to shRNA knockdown targeting genes encoding laminin 511 ( Results: Seven out of 52 individuals with IRC had autoantibodies against laminin 511-E8. Recombinant laminin 511-E8 led to differential expression of genes involved in secretion, barrier function, and inflammation. Knockdown of laminin 511 constituents increased toxic bile acid permeation and GCDC-induced apoptosis. Laminin 511-E8 treatment decreased toxic bile acid permeation and dose-dependently alleviated GCDC-induced apoptosis. Conclusions: Laminin 511-E8 is an autoantigen in subsets of individuals with IRC. Laminin 511 enhances cholangiocellular barrier function and protects cholangiocytes against T lymphocyte-induced barrier dysfunction, toxic bile acid permeation and bile acid-induced apoptosis. Impact and implications: A subset of patients with IgG4-related cholangitis (IRC) has autoantibodies against laminin 511-E8. In human cholangiocytes, laminin 511 protects against (T lymphocyte-induced) epithelial barrier dysfunction and hydrophobic bile acids. Laminin 511 and claudin 1 staining may be altered in extrahepatic bile ducts of patients with IRC who are anti-laminin 511-E8 positive. This makes it tempting to speculate that a decreased epithelial barrier function with attraction of immune cells and impaired bicarbonate secretion as a result of dysfunction of laminin 511 by autoantibody binding could potentially be a common systemic pathogenic mechanism in a subset of patients with IgG4-RD.
Language	English
Publishing date	2024-01-23
Publishing country	Netherlands
Document type	Journal Article
ISSN	2589-5559
ISSN (online)	2589-5559
DOI	10.1016/j.jhepr.2024.101015
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Article ; Online: Amino acid metabolism, transport and signalling in the liver revisited.

Paulusma, Coen C / Lamers, Wouter H / Broer, Stefan / van de Graaf, Stan F J

Biochemical pharmacology

2022 Volume 201, Page(s) 115074

Abstract: The liver controls the systemic exposure of amino acids entering via the gastro-intestinal tract. For most amino acids except branched chain amino acids, hepatic uptake is very efficient. This implies that the liver orchestrates amino acid metabolism and ...

Abstract	The liver controls the systemic exposure of amino acids entering via the gastro-intestinal tract. For most amino acids except branched chain amino acids, hepatic uptake is very efficient. This implies that the liver orchestrates amino acid metabolism and also controls systemic amino acid exposure. Although many amino acid transporters have been identified, cloned and investigated with respect to substrate specificity, transport mechanism, and zonal distribution, which of these players are involved in hepatocellular amino acid transport remains unclear. Here, we aim to provide a review of current insight into the molecular machinery of hepatic amino acid transport. Furthermore, we place this information in a comprehensive overview of amino acid transport, signalling and metabolism.
MeSH term(s)	Amino Acids/metabolism ; Amino Acids, Branched-Chain/metabolism ; Biological Transport ; Liver/metabolism ; Signal Transduction
Chemical Substances	Amino Acids ; Amino Acids, Branched-Chain
Language	English
Publishing date	2022-05-11
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.115074
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Article ; Online: Erratum to: "Hepatobiliary acid-base homeostasis: Insights from analogous secretory epithelia" (J Hepatol 2021; 74: 428-441).

Trampert, David C / van de Graaf, Stan F J / Jongejan, Aldo / Oude Elferink, Ronald P J / Beuers, Ulrich

Journal of hepatology

2021 Volume 75, Issue 2, Page(s) 497

Language	English
Publishing date	2021-05-13
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2021.05.002
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Article ; Online: IgG4-related cholangitis - a mimicker of fibrosing and malignant cholangiopathies.

Kersten, Remco / Trampert, David C / Herta, Toni / Hubers, Lowiek M / Maillette de Buy Wenniger, Lucas J / Verheij, Joanne / van de Graaf, Stan F J / Beuers, Ulrich

Journal of hepatology

2023 Volume 79, Issue 6, Page(s) 1502–1523

Abstract: IgG4-related cholangitis (IRC) is the major hepatobiliary manifestation of IgG4-related disease (IgG4-RD), a systemic fibroinflammatory disorder. The pathogenesis of IgG4-RD and IRC is currently viewed as multifactorial, as there is evidence of a genetic ...

Abstract	IgG4-related cholangitis (IRC) is the major hepatobiliary manifestation of IgG4-related disease (IgG4-RD), a systemic fibroinflammatory disorder. The pathogenesis of IgG4-RD and IRC is currently viewed as multifactorial, as there is evidence of a genetic predisposition while environmental factors, such as blue-collar work, are major risk factors. Various autoantigens have been described in IgG4-RD, including annexin A11 and laminin 511-E8, proteins which may exert a partially protective function in cholangiocytes by enhancing secretion and barrier function, respectively. For the other recently described autoantigens, galectin-3 and prohibitin 1, a distinct role in cholangiocytes appears less apparent. In relation to these autoantigens, oligoclonal expansions of IgG4
MeSH term(s)	Humans ; Immunoglobulin G ; Immunoglobulin G4-Related Disease/diagnosis ; Immunoglobulin G4-Related Disease/complications ; Cholangitis/etiology ; Autoantigens/therapeutic use ; Bile Duct Neoplasms ; Bile Ducts, Intrahepatic ; Cholangitis, Sclerosing ; Autoimmune Diseases
Chemical Substances	Immunoglobulin G ; Autoantigens
Language	English
Publishing date	2023-08-18
Publishing country	Netherlands
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2023.08.005
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Zs.A 2027: Show issues

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Article ; Online: Targeting the Four Pillars of Enterohepatic Bile Salt Cycling; Lessons From Genetics and Pharmacology.

Kunst, Roni F / Verkade, Henkjan J / Oude Elferink, Ronald P J / van de Graaf, Stan F J

Hepatology (Baltimore, Md.)

2021 Volume 73, Issue 6, Page(s) 2577–2585

Abstract: Bile salts play a pivotal role in lipid homeostasis, are sensed by specialized receptors, and have been implicated in various disorders affecting the gut or liver. They may play a role either as culprit or as potential panacea. Four very efficient ... ...

Abstract	Bile salts play a pivotal role in lipid homeostasis, are sensed by specialized receptors, and have been implicated in various disorders affecting the gut or liver. They may play a role either as culprit or as potential panacea. Four very efficient transporters mediate most of the hepatic and intestinal bile salt uptake and efflux, and are each essential for the efficient enterohepatic circulation of bile salts. Starting from the intestinal lumen, conjugated bile salts cross the otherwise impermeable lipid bilayer of (primarily terminal ileal) enterocytes through the apical sodium-dependent bile acid transporter (gene SLC10A2) and leave the enterocyte through the basolateral heteromeric organic solute transporter, which consists of an alpha and beta subunit (encoded by SLC51A and SLC51B). The Na
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B, Member 11/genetics ; ATP Binding Cassette Transporter, Subfamily B, Member 11/metabolism ; Animals ; Bile Acids and Salts/metabolism ; Biological Transport, Active/drug effects ; Biological Transport, Active/physiology ; Drug Development ; Enterohepatic Circulation/drug effects ; Enterohepatic Circulation/physiology ; Humans ; Membrane Transport Proteins/genetics ; Membrane Transport Proteins/metabolism ; Organic Anion Transporters, Sodium-Dependent/antagonists & inhibitors ; Organic Anion Transporters, Sodium-Dependent/genetics ; Organic Anion Transporters, Sodium-Dependent/metabolism ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Symporters/antagonists & inhibitors ; Symporters/genetics ; Symporters/metabolism
Chemical Substances	ABCB11 protein, human ; ATP Binding Cassette Transporter, Subfamily B, Member 11 ; Bile Acids and Salts ; Membrane Transport Proteins ; Organic Anion Transporters, Sodium-Dependent ; Receptors, G-Protein-Coupled ; SLC52A1 protein, human ; Symporters ; SLC51B protein, human ; sodium-bile acid cotransporter (145420-23-1)
Language	English
Publishing date	2021-05-24
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.31651
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