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  1. AU=Fausther Michel
  2. AU="Arrate, Clara"
  3. AU="Tarrach, Klaus"
  4. AU="Coburn, Bryan A"
  5. AU="Fieke Mooren"
  6. AU=Lubitz Steven A.
  7. AU=Chattopadhyay Sanchari
  8. AU=Ghanbari Behzad
  9. AU="Desmecht, Daniel"
  10. AU="Juškov, A. N"
  11. AU="Bach, Francis"
  12. AU="Afşin, Emine"
  13. AU="McLeod, Jonathan"
  14. AU=Srensen Morten Drby
  15. AU=de Noronha Lucia
  16. AU=Robinson Jennifer G
  17. AU=CHIACO JOHN MICHAEL S. CHUA
  18. AU="Simon, Benedikt"
  19. AU="Zhao, Andong"
  20. AU="Zhao, Tianshi"
  21. AU="Morris, Helen"

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

    Fausther, Michel

    American journal of physiology. Gastrointestinal and liver physiology

    2018  Band 315, Heft 1, Seite(n) 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-Begriff(e) Adenosine/metabolism ; Disease Progression ; Humans ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Myofibroblasts/metabolism ; Signal Transduction
    Chemische Substanzen Adenosine (K72T3FS567)
    Sprache Englisch
    Erscheinungsdatum 2018-03-29
    Erscheinungsland United States
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Beyond scar formation: portal myofibroblast-mediated angiogenesis in the fibrotic liver.

    Fausther, Michel / Dranoff, Jonathan A

    Hepatology (Baltimore, Md.)

    2015  Band 61, Heft 3, Seite(n) 766–768

    Mesh-Begriff(e) Animals ; Cell-Derived Microparticles/secretion ; Humans ; Liver/cytology ; Liver Cirrhosis/etiology ; Male ; Myofibroblasts/physiology ; Vascular Remodeling
    Sprache Englisch
    Erscheinungsdatum 2015-03
    Erscheinungsland United States
    Dokumenttyp Comment ; Editorial
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.27653
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: Integrins, myofibroblasts, and organ fibrosis.

    Fausther, Michel / Dranoff, Jonathan A

    Hepatology (Baltimore, Md.)

    2014  Band 60, Heft 2, Seite(n) 756–758

    Mesh-Begriff(e) Animals ; Female ; Integrin alphaV/metabolism ; Kidney/pathology ; Kidney Diseases/genetics ; Liver Cirrhosis/genetics ; Male ; Pulmonary Fibrosis/genetics
    Chemische Substanzen Integrin alphaV
    Sprache Englisch
    Erscheinungsdatum 2014-05-09
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.27155
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; 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  Band 12, Heft 9, Seite(n) 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-Begriff(e) 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
    Chemische Substanzen GPI-Linked Proteins ; Protein Isoforms ; mesothelin (J27WDC343N)
    Sprache Englisch
    Erscheinungsdatum 2017-09-12
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0184499
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; 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  Band 2017, Seite(n) 6824762

    Mesh-Begriff(e) Animals ; Cellular Microenvironment ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology
    Sprache Englisch
    Erscheinungsdatum 2017-02-16
    Erscheinungsland United States
    Dokumenttyp Editorial
    ZDB-ID 2698540-8
    ISSN 2314-6141 ; 2314-6133
    ISSN (online) 2314-6141
    ISSN 2314-6133
    DOI 10.1155/2017/6824762
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Liver myofibroblasts of murine origins express mesothelin

    Michel Fausther / Elise G Lavoie / Jonathan A Dranoff

    PLoS ONE, Vol 12, Iss 9, p e

    Identification of novel rat mesothelin splice variants.

    2017  Band 0184499

    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.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2017-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel: 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
    Sprache Englisch
    Erscheinungsdatum 2017--11
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 1151108-4
    ISSN 1052-2166 ; 1052-2116
    ISSN 1052-2166 ; 1052-2116
    DOI 10.3727/105221617X15042723767876
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; 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  Band 13, Heft 4, Seite(n) 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-Begriff(e) 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
    Chemische Substanzen DNA-Binding Proteins ; Elf2 protein, mouse ; Transcription Factors ; 5'-Nucleotidase (EC 3.1.3.5)
    Sprache Englisch
    Erscheinungsdatum 2017-06-30
    Erscheinungsland Netherlands
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Contribution of Liver Nonparenchymal Cells to Hepatic Fibrosis

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

    BioMed Research International, Vol

    Interactions with the Local Microenvironment

    2017  Band 2017

    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2017-01-01T00:00:00Z
    Verlag Hindawi Limited
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Extracellular nucleosides and nucleotides regulate liver functions via a complex system of membrane proteins.

    Fausther, Michel / Sévigny, Jean

    Comptes rendus biologies

    2011  Band 334, Heft 2, Seite(n) 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-Begriff(e) 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
    Chemische Substanzen 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.-)
    Sprache Französisch
    Erscheinungsdatum 2011-02
    Erscheinungsland France
    Dokumenttyp 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
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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