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Article ; Online: Extracellular adenosine: a critical signal in liver fibrosis.

Fausther, Michel

American journal of physiology. Gastrointestinal and liver physiology

2018 Volume 315, Issue 1, Page(s) G12–G19

Abstract: Extracellular adenosine nucleoside is a potent, endogenous mediator that signals through specific G protein-coupled receptors, and exerts pleiotropic effects on liver physiology, in health and disease. Particularly, adenosinergic or adenosine-mediated ... ...

Abstract	Extracellular adenosine nucleoside is a potent, endogenous mediator that signals through specific G protein-coupled receptors, and exerts pleiotropic effects on liver physiology, in health and disease. Particularly, adenosinergic or adenosine-mediated signaling pathways impact the progression of hepatic fibrosis, a common feature of chronic liver diseases, through regulation of matrix deposition by liver myofibroblasts. This review examines the current lines of evidence on adenosinergic regulation of liver fibrosis and myofibroblasts, identifies unanswered research questions, and proposes important future areas of investigation.
MeSH term(s)	Adenosine/metabolism ; Disease Progression ; Humans ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Myofibroblasts/metabolism ; Signal Transduction
Chemical Substances	Adenosine (K72T3FS567)
Language	English
Publishing date	2018-03-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00006.2018
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Article ; Online: Beyond scar formation: portal myofibroblast-mediated angiogenesis in the fibrotic liver.

Fausther, Michel / Dranoff, Jonathan A

Hepatology (Baltimore, Md.)

2015 Volume 61, Issue 3, Page(s) 766–768

MeSH term(s)	Animals ; Cell-Derived Microparticles/secretion ; Humans ; Liver/cytology ; Liver Cirrhosis/etiology ; Male ; Myofibroblasts/physiology ; Vascular Remodeling
Language	English
Publishing date	2015-03
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.27653
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Zs.A 1660: Show issues

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Article ; Online: Integrins, myofibroblasts, and organ fibrosis.

Fausther, Michel / Dranoff, Jonathan A

Hepatology (Baltimore, Md.)

2014 Volume 60, Issue 2, Page(s) 756–758

MeSH term(s)	Animals ; Female ; Integrin alphaV/metabolism ; Kidney/pathology ; Kidney Diseases/genetics ; Liver Cirrhosis/genetics ; Male ; Pulmonary Fibrosis/genetics
Chemical Substances	Integrin alphaV
Language	English
Publishing date	2014-05-09
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.27155
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Zs.A 1660: Show issues

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Article ; Online: Liver myofibroblasts of murine origins express mesothelin: Identification of novel rat mesothelin splice variants.

Fausther, Michel / G Lavoie, Elise / Dranoff, Jonathan A

PloS one

2017 Volume 12, Issue 9, Page(s) e0184499

Abstract: Liver myofibroblasts are specialized effector cells that drive hepatic fibrosis, a hallmark process of chronic liver diseases, leading to progressive scar formation and organ failure. Liver myofibroblasts are increasingly recognized as heterogeneous with ...

Abstract	Liver myofibroblasts are specialized effector cells that drive hepatic fibrosis, a hallmark process of chronic liver diseases, leading to progressive scar formation and organ failure. Liver myofibroblasts are increasingly recognized as heterogeneous with regards to their origin, phenotype, and functions. For instance, liver myofibroblasts express cell markers that are universally represented such as, ItgαV and Pdgfrβ, or restricted to a given subpopulation such as, Lrat exclusively expressed in hepatic stellate cells, and Gpm6a in mesothelial cells. To study liver myofibroblasts in vitro, we have previously generated and characterized a SV40-immortalized polyclonal rat activated portal fibroblast cell line called RGF-N2 expressing multiple mesothelin mRNA transcripts. Mesothelin, a cell-surface molecule expressed in normal mesothelial cells and overexpressed in several cancers such as, mesothelioma and cholangiocarcinoma, was recently identified as a key regulator of portal myofibroblast proliferation, and fibrosis progression in the setting of chronic cholestatic liver disease. Here, we identify novel mesothelin splice variants expressed in rat activated portal fibroblasts. RGF-N2 portal fibroblast cDNA was used as template for insertion of hemagglutinin tag consensus sequence into the complete open reading frame of rat mesothelin variant coding sequences by extension PCR. Purified amplicons were subsequently cloned into an expression vector for in vitro translation and transfection in monkey COS7 fibroblasts, before characterization of fusion proteins by immunoblot and immunofluorescence. We show that rat activated portal fibroblasts, hepatic stellate cells, and cholangiocarcinoma cells express wild-type mesothelin and additional splice variants, while mouse activated hepatic stellate cells appear to only express wild-type mesothelin. Notably, rat mesothelin splice variants differ from the wild-type isoform by their protein properties and cellular distribution in transfected COS7 fibroblasts. We conclude that mesothelin is a marker of activated murine liver myofibroblasts. Mesothelin gene expression and regulation may be critical in liver myofibroblasts functions and fibrosis progression.
MeSH term(s)	Animals ; COS Cells ; Cell Line, Tumor ; Cells, Cultured ; Chlorocebus aethiops ; GPI-Linked Proteins/genetics ; GPI-Linked Proteins/metabolism ; Hepatic Stellate Cells/metabolism ; Liver/cytology ; Liver/metabolism ; Male ; Mice ; Myofibroblasts/metabolism ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; RNA Splicing ; Rats ; Rats, Sprague-Dawley
Chemical Substances	GPI-Linked Proteins ; Protein Isoforms ; mesothelin (J27WDC343N)
Language	English
Publishing date	2017-09-12
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0184499
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Article ; Online: Contribution of Liver Nonparenchymal Cells to Hepatic Fibrosis: Interactions with the Local Microenvironment.

Fausther, Michel / Pritchard, Michele T / Popov, Yury V / Bridle, Kim

BioMed research international

2017 Volume 2017, Page(s) 6824762

MeSH term(s)	Animals ; Cellular Microenvironment ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology
Language	English
Publishing date	2017-02-16
Publishing country	United States
Document type	Editorial
ZDB-ID	2698540-8
ISSN	2314-6141 ; 2314-6133
ISSN (online)	2314-6141
ISSN	2314-6133
DOI	10.1155/2017/6824762
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Article: The cholangiocyte adenosine-IL6 axis regulates survival during biliary cirrhosis.

Lavoie, Elise / Fausther, Michel / Goree, Jessica / Dranoff, Jonathan A

Gene expression

2017

Abstract: BACKGROUND AND AIMSEpithelial response to injury is critical to the pathogenesis of biliary cirrhosis, and IL6 has been suggested as a mediator of this phenomenon. Several liver cell types can secrete IL6 following activation by various signaling ... ...

Abstract	BACKGROUND AND AIMSEpithelial response to injury is critical to the pathogenesis of biliary cirrhosis, and IL6 has been suggested as a mediator of this phenomenon. Several liver cell types can secrete IL6 following activation by various signaling molecules including circulating adenosine. The aims of this study are to assess whether adenosine can induce IL6 secretion by cholangiocytes via the A2b adenosine receptor (A2bAR) and determine the effect of A2bAR-sensitive IL6 release on injury response in biliary cirrhosis.METHODSHuman normal cholangiocyte H69 cells were used for in vitro studies to determine the mechanism by which adenosine and the A2bAR induces release of IL6. In vivo, control and A2bAR-deficient mice were used to determine the roles of A2bAR-sensitive IL6 release in biliary cirrhosis induced by common bile duct ligation (BDL). Additionally, the response to exogenous IL6 was assessed in C57BL/6 and A2bAR-deficient mice.RESULTSAdenosine induced IL6 mRNA expression and protein secretion via A2bAR activation. Although activation of A2bAR induced cAMP and intracellular Ca
Language	English
Publishing date	2017--11
Publishing country	United States
Document type	Journal Article
ZDB-ID	1151108-4
ISSN	1052-2166 ; 1052-2116
ISSN	1052-2166 ; 1052-2116
DOI	10.3727/105221617X15042723767876
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Zs.A 3683: Show issues

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Article ; Online: An Elf2-like transcription factor acts as repressor of the mouse ecto-5'-nucleotidase gene expression in hepatic myofibroblasts.

Fausther, Michel / Lavoie, Elise G / Goree, Jessica R / Dranoff, Jonathan A

Purinergic signalling

2017 Volume 13, Issue 4, Page(s) 417–428

Abstract: Hepatic fibrosis represents a pathological wound healing and tissue repair process triggered in response to chronic liver injury. A heterogeneous population of activated non-parenchymal liver cells, known as liver myofibroblasts, functions as the ... ...

Abstract	Hepatic fibrosis represents a pathological wound healing and tissue repair process triggered in response to chronic liver injury. A heterogeneous population of activated non-parenchymal liver cells, known as liver myofibroblasts, functions as the effector cells in hepatic fibrosis. Upon activation, liver myofibroblasts become fibrogenic, acquiring contractile properties and increasing collagen production capacity, while developing enhanced sensitivity to endogenous molecules and factors released in the local microenvironment. Hepatic extracellular adenosine is a bioactive small molecule, increasingly recognized as an important regulator of liver myofibroblast functions, and an important mediator in the pathogenesis of liver fibrosis overall. Remarkably, ecto-5'-nucleotidase/Nt5e/Cd73 enzyme, which accounts for the dominant adenosine-generating activity in the extracellular medium, is expressed by activated liver myofibroblasts. However, the molecular signals regulating Nt5e gene expression in liver myofibroblasts remain poorly understood. Here, we show that activated mouse liver myofibroblasts express Nt5e gene products and characterize the putative Nt5e minimal promoter in the mouse species. We describe the existence of an enhancer sequence upstream of the mouse Nt5e minimal promoter and establish that the mouse Nt5e minimal promoter transcriptional activity is negatively regulated by an Elf2-like Ets-related transcription factor in activated mouse liver myofibroblasts.
MeSH term(s)	5'-Nucleotidase/biosynthesis ; Animals ; DNA-Binding Proteins/metabolism ; Gene Expression Regulation/physiology ; Liver Cirrhosis/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myofibroblasts/metabolism ; Transcription Factors/metabolism
Chemical Substances	DNA-Binding Proteins ; Elf2 protein, mouse ; Transcription Factors ; 5'-Nucleotidase (EC 3.1.3.5)
Language	English
Publishing date	2017-06-30
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2172143-9
ISSN	1573-9546 ; 1573-9538
ISSN (online)	1573-9546
ISSN	1573-9538
DOI	10.1007/s11302-017-9570-7
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Article ; Online: Extracellular nucleosides and nucleotides regulate liver functions via a complex system of membrane proteins.

Fausther, Michel / Sévigny, Jean

Comptes rendus biologies

2011 Volume 334, Issue 2, Page(s) 100–117

Abstract: Nucleosides and nucleotides are now considered as extracellular signalling molecules, like neurotransmitters and hormones. Hepatic cells, amongst other cells, ubiquitously express specific transmembrane receptors that transduce the physiological signals ... ...

Abstract	Nucleosides and nucleotides are now considered as extracellular signalling molecules, like neurotransmitters and hormones. Hepatic cells, amongst other cells, ubiquitously express specific transmembrane receptors that transduce the physiological signals induced by extracellular nucleosides and nucleotides, as well as various cell surface enzymes that regulate the levels of these mediators in the extracellular medium. Here, we cover various aspects of the signalling pathways initiated by extracellular nucleosides and nucleotides in the liver, and discuss their overall impact on hepatic physiology.
MeSH term(s)	Adenosine Triphosphate/physiology ; Animals ; Extracellular Fluid/physiology ; Hepatocytes/metabolism ; Humans ; Liver/metabolism ; Liver/physiology ; Membrane Proteins/physiology ; Mice ; Nucleosides/physiology ; Nucleotides/physiology ; Phosphoric Diester Hydrolases/metabolism ; Phosphoric Monoester Hydrolases/metabolism ; Pyrophosphatases/metabolism ; Receptors, Purinergic/physiology ; Signal Transduction/physiology
Chemical Substances	Membrane Proteins ; Nucleosides ; Nucleotides ; Receptors, Purinergic ; Adenosine Triphosphate (8L70Q75FXE) ; Phosphoric Monoester Hydrolases (EC 3.1.3.2) ; Phosphoric Diester Hydrolases (EC 3.1.4.-) ; Pyrophosphatases (EC 3.6.1.-)
Language	French
Publishing date	2011-02
Publishing country	France
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2072863-3
ISSN	1768-3238 ; 1631-0691
ISSN (online)	1768-3238
ISSN	1631-0691
DOI	10.1016/j.crvi.2010.12.005
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Zs.B 1008: Show issues

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Article ; Online: New insights on the pathogenesis of biliary cirrhosis provided by studies in FXR knockout mice.

Fausther, Michel / Dranoff, Jonathan A

Journal of hepatology

2011 Volume 55, Issue 4, Page(s) 939–940

Abstract: The nuclear bile acid receptor, farnesoid X receptor (FXR), may play a pivotal role in liver fibrosis. We tested the impact of genetic FXR ablation in four different mouse models. Hepatic fibrosis was induced in wild-type and FXR knock-out mice (FXR((-/-) ...

Abstract	The nuclear bile acid receptor, farnesoid X receptor (FXR), may play a pivotal role in liver fibrosis. We tested the impact of genetic FXR ablation in four different mouse models. Hepatic fibrosis was induced in wild-type and FXR knock-out mice (FXR((-/-))) by CCl(4) intoxication, 3,5-diethoxycarbonyl-1,4-dihydrocollidine feeding, common bile duct ligation, or Schistosoma mansoni (S.m.)-infection. In addition, we determined nuclear receptor expression levels (FXR, pregnane X receptor (PXR), vitamin D receptor, constitutive androstane receptor (CAR), small heterodimer partner (SHP)) in mouse hepatic stellate cells (HSCs), portal myofibroblasts (MFBs), and human HSCs. Cell type-specific FXR protein expression was determined by immunohistochemistry in five mouse models and prototypic human fibrotic liver diseases. Expression of nuclear receptors was much lower in mouse and human HSCs/MFBs compared with total liver expression with the exception of vitamin D receptor. FXR protein was undetectable in mouse and human HSCs and MFBs. FXR loss had no effect in CCl(4)-intoxicated and S.m.-infected mice, but significantly decreased liver fibrosis of the biliary type (common bile duct ligation, 3,5-diethoxycarbonyl-1,4-dihydrocollidine). These data suggest that FXR loss significantly reduces fibrosis of the biliary type, but has no impact on non-cholestatic liver fibrosis. Since there is no FXR expression in HSCs and MFBs in liver fibrosis, our data indicate that these cells may not represent direct therapeutic targets for FXR ligands.
Language	English
Publishing date	2011-05-11
Publishing country	Netherlands
Document type	Comment ; Journal Article
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2011.04.013
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Zs.A 2027: Show issues

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Article ; Online: Ticlopidine in its prodrug form is a selective inhibitor of human NTPDase1.

Lecka, Joanna / Fausther, Michel / Künzli, Beat / Sévigny, Jean

Mediators of inflammation

2014 Volume 2014, Page(s) 547480

Abstract: Nucleoside triphosphate diphosphohydrolase-1 (NTPDase1), like other ectonucleotidases, controls extracellular nucleotide levels and consequently their (patho)physiological responses such as in thrombosis, inflammation, and cancer. Selective NTPDase1 ... ...

Abstract	Nucleoside triphosphate diphosphohydrolase-1 (NTPDase1), like other ectonucleotidases, controls extracellular nucleotide levels and consequently their (patho)physiological responses such as in thrombosis, inflammation, and cancer. Selective NTPDase1 inhibitors would therefore be very useful. We previously observed that ticlopidine in its prodrug form, which does not affect P2 receptor activity, inhibited the recombinant form of human NTPDase1 (K i = 14 μM). Here we tested whether ticlopidine can be used as a selective inhibitor of NTPDase1. We confirmed that ticlopidine inhibits NTPDase1 in different forms and in different assays. The ADPase activity of intact HUVEC as well as of COS-7 cells transfected with human NTPDase1 was strongly inhibited by 100 µM ticlopidine, 99 and 86%, respectively. Ticlopidine (100 µM) completely inhibited the ATPase activity of NTPDase1 in situ as shown by enzyme histochemistry with human liver and pancreas sections. Ticlopidine also inhibited the activity of rat and mouse NTPDase1 and of potato apyrase. At 100 µM ticlopidine did not affect the activity of human NTPDase2, NTPDase3, and NTPDase8, nor of NPP1 and NPP3. Weak inhibition (10-20%) of NTPDase3 and -8 was observed at 1 mM ticlopidine. These results show that ticlopidine is a specific inhibitor of NTPDase1 that can be used in enzymatic and histochemistry assays.
MeSH term(s)	Adenosine Triphosphatases/metabolism ; Animals ; Antigens, CD/metabolism ; Apyrase/metabolism ; COS Cells ; Chlorocebus aethiops ; Enzyme Activation/drug effects ; Enzyme Inhibitors/chemistry ; Enzyme Inhibitors/pharmacology ; Human Umbilical Vein Endothelial Cells ; Humans ; Pyrophosphatases/metabolism ; Ticlopidine/chemistry ; Ticlopidine/pharmacology
Chemical Substances	Antigens, CD ; Enzyme Inhibitors ; Adenosine Triphosphatases (EC 3.6.1.-) ; Pyrophosphatases (EC 3.6.1.-) ; ectoATPase (EC 3.6.1.-) ; nucleoside-triphosphate diphosphohydrolase 3 (EC 3.6.1.-) ; Apyrase (EC 3.6.1.5) ; CD39 antigen (EC 3.6.1.5) ; Ticlopidine (OM90ZUW7M1)
Language	English
Publishing date	2014-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1137605-3
ISSN	1466-1861 ; 0962-9351
ISSN (online)	1466-1861
ISSN	0962-9351
DOI	10.1155/2014/547480
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