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Article ; Online: The immediate-early protein 1 of human herpesvirus 6B interacts with NBS1 and inhibits ATM signaling.

Collin, Vanessa / Biquand, Élise / Tremblay, Vincent / Lavoie, Élise G / Blondeau, Andréanne / Gravel, Annie / Galloy, Maxime / Lashgari, Anahita / Dessapt, Julien / Côté, Jacques / Flamand, Louis / Fradet-Turcotte, Amélie

EMBO reports

2024 Volume 25, Issue 2, Page(s) 725–744

Abstract: Viral infection often trigger an ATM serine/threonine kinase (ATM)-dependent DNA damage response in host cells that suppresses viral replication. Viruses evolved different strategies to counteract this antiviral surveillance system. Here, we report that ... ...

Abstract	Viral infection often trigger an ATM serine/threonine kinase (ATM)-dependent DNA damage response in host cells that suppresses viral replication. Viruses evolved different strategies to counteract this antiviral surveillance system. Here, we report that human herpesvirus 6B (HHV-6B) infection causes genomic instability by suppressing ATM signaling in host cells. Expression of immediate-early protein 1 (IE1) phenocopies this phenotype and blocks homology-directed double-strand break repair. Mechanistically, IE1 interacts with NBS1, and inhibits ATM signaling through two distinct domains. HHV-6B seems to efficiently inhibit ATM signaling as further depletion of either NBS1 or ATM do not significantly boost viral replication in infected cells. Interestingly, viral integration of HHV-6B into the host's telomeres is not strictly dependent on NBS1, challenging current models where integration occurs through homology-directed repair. Given that spontaneous IE1 expression has been detected in cells of subjects with inherited chromosomally-integrated form of HHV-6B (iciHHV-6B), a condition associated with several health conditions, our results raise the possibility of a link between genomic instability and the development of iciHHV-6-associated diseases.
MeSH term(s)	Humans ; Herpesvirus 6, Human/genetics ; Herpesvirus 6, Human/metabolism ; Roseolovirus Infections/genetics ; Immediate-Early Proteins/genetics ; Immediate-Early Proteins/metabolism ; Virus Integration ; Genomic Instability ; Ataxia Telangiectasia Mutated Proteins/genetics ; Ataxia Telangiectasia Mutated Proteins/metabolism
Chemical Substances	Immediate-Early Proteins ; ATM protein, human (EC 2.7.11.1) ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1)
Language	English
Publishing date	2024-01-02
Publishing country	England
Document type	Journal Article
ZDB-ID	2020896-0
ISSN	1469-3178 ; 1469-221X
ISSN (online)	1469-3178
ISSN	1469-221X
DOI	10.1038/s44319-023-00035-z
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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: 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 Volume 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 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.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: A Simple and Efficient Genetic Immunization Protocol for the Production of Highly Specific Polyclonal and Monoclonal Antibodies against the Native Form of Mammalian Proteins.

Pelletier, Julie / Agonsanou, Hervé / Manica, Fabiana / G Lavoie, Elise / Salem, Mabrouka / Luyindula, Patrick / Babou Kammoe, Romuald Brice / Sévigny, Jean

International journal of molecular sciences

2020 Volume 21, Issue 19

Abstract: We have generated polyclonal and monoclonal antibodies by genetic immunization over the last two decades. In this paper, we present our most successful methodology acquired over these years and present the animals in which we obtained the highest rates ... ...

Abstract	We have generated polyclonal and monoclonal antibodies by genetic immunization over the last two decades. In this paper, we present our most successful methodology acquired over these years and present the animals in which we obtained the highest rates of success. The technique presented is convenient, easy, affordable, and generates antibodies against mammalian proteins in their native form. This protocol requires neither expensive equipment, such as a gene gun, nor sophisticated techniques such as the conjugation of gold microspheres, electroporation, or surgery to inject in lymph nodes. The protocol presented uses simply the purified plasmid expressing the protein of interest under a strong promoter, which is injected at intramuscular and intradermal sites. This technique was tested in five species. Guinea pigs were the animals of choice for the production of polyclonal antibodies. Monoclonal antibodies could be generated in mice by giving, as a last injection, a suspension of transfected cells. The antibodies detected their antigens in their native forms. They were highly specific with very low non-specific background levels, as assessed by immune-blots, immunocytochemistry, immunohistochemistry and flow cytometry. We present herein a detailed and simple procedure to successfully raise specific antibodies against native proteins.
MeSH term(s)	Animals ; Antibodies, Monoclonal/biosynthesis ; COS Cells ; Chlorocebus aethiops ; Cricetinae ; DNA, Complementary/immunology ; Female ; Guinea Pigs ; HEK293 Cells ; Humans ; Immunization ; Mice ; Mice, Inbred BALB C ; Proteins/immunology ; Rabbits ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Antibodies, Monoclonal ; DNA, Complementary ; Proteins
Language	English
Publishing date	2020-09-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21197074
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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: FIRRM cooperates with FIGNL1 to promote RAD51 disassembly during DNA repair.

Pinedo-Carpio, Edgar / Dessapt, Julien / Beneyton, Adèle / Sacre, Lauralicia / Bérubé, Marie-Anne / Villot, Romain / Lavoie, Elise G / Coulombe, Yan / Blondeau, Andréanne / Boulais, Jonathan / Malina, Abba / Luo, Vincent M / Lazaratos, Anna-Maria / Côté, Jean-François / Mallette, Frédérick A / Guarné, Alba / Masson, Jean-Yves / Fradet-Turcotte, Amélie / Orthwein, Alexandre

Science advances

2023 Volume 9, Issue 32, Page(s) eadf4082

Abstract: Interstrand DNA cross-links (ICLs) represent complex lesions that compromise genomic stability. Several pathways have been involved in ICL repair, but the extent of factors involved in the resolution of ICL-induced DNA double-strand breaks (DSBs) remains ...

Abstract	Interstrand DNA cross-links (ICLs) represent complex lesions that compromise genomic stability. Several pathways have been involved in ICL repair, but the extent of factors involved in the resolution of ICL-induced DNA double-strand breaks (DSBs) remains poorly defined. Using CRISPR-based genomics, we identified FIGNL1 interacting regulator of recombination and mitosis (FIRRM) as a sensitizer of the ICL-inducing agent mafosfamide. Mechanistically, we showed that FIRRM, like its interactor Fidgetin like 1 (FIGNL1), contributes to the resolution of RAD51 foci at ICL-induced DSBs. While the stability of FIGNL1 and FIRRM is interdependent, expression of a mutant of FIRRM (∆WCF), which stabilizes the protein in the absence of FIGNL1, allows the resolution of RAD51 foci and cell survival, suggesting that FIRRM has FIGNL1-independent function during DNA repair. In line with this model, FIRRM binds preferentially single-stranded DNA in vitro, raising the possibility that it directly contributes to RAD51 disassembly by interacting with DNA. Together, our findings establish FIRRM as a promoting factor of ICL repair.
MeSH term(s)	Rad51 Recombinase/genetics ; Rad51 Recombinase/metabolism ; DNA Repair ; Proteins/genetics ; DNA/genetics ; Mitosis
Chemical Substances	Rad51 Recombinase (EC 2.7.7.-) ; Proteins ; DNA (9007-49-2)
Language	English
Publishing date	2023-08-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2810933-8
ISSN	2375-2548 ; 2375-2548
ISSN (online)	2375-2548
ISSN	2375-2548
DOI	10.1126/sciadv.adf4082
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Article ; Online: A Simple and Efficient Genetic Immunization Protocol for the Production of Highly Specific Polyclonal and Monoclonal Antibodies against the Native Form of Mammalian Proteins

Julie Pelletier / Hervé Agonsanou / Fabiana Manica / Elise G. Lavoie / Mabrouka Salem / Patrick Luyindula / Romuald Brice Babou Kammoe / Jean Sévigny

International Journal of Molecular Sciences, Vol 21, Iss 7074, p

2020 Volume 7074

Abstract	We have generated polyclonal and monoclonal antibodies by genetic immunization over the last two decades. In this paper, we present our most successful methodology acquired over these years and present the animals in which we obtained the highest rates of success. The technique presented is convenient, easy, affordable, and generates antibodies against mammalian proteins in their native form. This protocol requires neither expensive equipment, such as a gene gun, nor sophisticated techniques such as the conjugation of gold microspheres, electroporation, or surgery to inject in lymph nodes. The protocol presented uses simply the purified plasmid expressing the protein of interest under a strong promoter, which is injected at intramuscular and intradermal sites. This technique was tested in five species. Guinea pigs were the animals of choice for the production of polyclonal antibodies. Monoclonal antibodies could be generated in mice by giving, as a last injection, a suspension of transfected cells. The antibodies detected their antigens in their native forms. They were highly specific with very low non-specific background levels, as assessed by immune-blots, immunocytochemistry, immunohistochemistry and flow cytometry. We present herein a detailed and simple procedure to successfully raise specific antibodies against native proteins.
Keywords	immunization ; antibody ; protocol ; guinea pig ; cDNA ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	616
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Human papillomavirus E7 oncoprotein targets RNF168 to hijack the host DNA damage response.

Sitz, Justine / Blanchet, Sophie Anne / Gameiro, Steven F / Biquand, Elise / Morgan, Tia M / Galloy, Maxime / Dessapt, Julien / Lavoie, Elise G / Blondeau, Andréanne / Smith, Brandon C / Mymryk, Joe S / Moody, Cary A / Fradet-Turcotte, Amélie

Proceedings of the National Academy of Sciences of the United States of America

2019 Volume 116, Issue 39, Page(s) 19552–19562

Abstract: High-risk human papillomaviruses (HR-HPVs) promote cervical cancer as well as a subset of anogenital and head and neck cancers. Due to their limited coding capacity, HPVs hijack the host cell's DNA replication and repair machineries to replicate their ... ...

Abstract	High-risk human papillomaviruses (HR-HPVs) promote cervical cancer as well as a subset of anogenital and head and neck cancers. Due to their limited coding capacity, HPVs hijack the host cell's DNA replication and repair machineries to replicate their own genomes. How this host-pathogen interaction contributes to genomic instability is unknown. Here, we report that HPV-infected cancer cells express high levels of RNF168, an E3 ubiquitin ligase that is critical for proper DNA repair following DNA double-strand breaks, and accumulate high numbers of 53BP1 nuclear bodies, a marker of genomic instability induced by replication stress. We describe a mechanism by which HPV E7 subverts the function of RNF168 at DNA double-strand breaks, providing a rationale for increased homology-directed recombination in E6/E7-expressing cervical cancer cells. By targeting a new regulatory domain of RNF168, E7 binds directly to the E3 ligase without affecting its enzymatic activity. As RNF168 knockdown impairs viral genome amplification in differentiated keratinocytes, we propose that E7 hijacks the E3 ligase to promote the viral replicative cycle. This study reveals a mechanism by which tumor viruses reshape the cellular response to DNA damage by manipulating RNF168-dependent ubiquitin signaling. Importantly, our findings reveal a pathway by which HPV may promote the genomic instability that drives oncogenesis.
MeSH term(s)	Cell Line, Tumor ; DNA Breaks, Double-Stranded ; DNA Repair ; Female ; Genomic Instability ; Homologous Recombination ; Host-Pathogen Interactions ; Humans ; Papillomaviridae/metabolism ; Papillomavirus E7 Proteins/genetics ; Papillomavirus E7 Proteins/metabolism ; Papillomavirus Infections/genetics ; Papillomavirus Infections/virology ; Signal Transduction ; Tumor Suppressor p53-Binding Protein 1/metabolism ; Ubiquitin/genetics ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Uterine Cervical Neoplasms/virology
Chemical Substances	Papillomavirus E7 Proteins ; TP53BP1 protein, human ; Tumor Suppressor p53-Binding Protein 1 ; Ubiquitin ; RNF168 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27)
Language	English
Publishing date	2019-09-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1906102116
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Zs.A 1148: Show issues

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Article ; Online: Reduction in SNAP-23 Alters Microfilament Organization in Myofibrobastic Hepatic Stellate Cells.

Eubanks, Haleigh B / Lavoie, Elise G / Goree, Jessica / Kamykowski, Jeffrey A / Gokden, Neriman / Fausther, Michel / Dranoff, Jonathan A

Gene expression

2019 Volume 20, Issue 1, Page(s) 25–37

Abstract: Hepatic stellate cells (HSC) are critical effector cells of liver fibrosis. In the injured liver, HSC differentiate into a myofibrobastic phenotype. A critical feature distinguishing myofibroblastic from quiescent HSC is cytoskeletal reorganization. ... ...

Abstract	Hepatic stellate cells (HSC) are critical effector cells of liver fibrosis. In the injured liver, HSC differentiate into a myofibrobastic phenotype. A critical feature distinguishing myofibroblastic from quiescent HSC is cytoskeletal reorganization. Soluble NSF attachment receptor (SNARE) proteins are important in trafficking of newly synthesized proteins to the plasma membrane for release into the extracellular environment. The goals of this project were to determine the expression of specific SNARE proteins in myofibroblastic HSC and to test whether their alteration changed the HSC phenotype in vitro and progression of liver fibrosis in vivo. We found that HSC lack the t-SNARE protein, SNAP-25, but express a homologous protein, SNAP-23. Downregulation of SNAP-23 in HSC induced reduction in polymerization and disorganization of the actin cytoskeleton associated with loss of cell movement. In contrast, reduction in SNAP-23 in mice by monogenic deletion delayed but did not prevent progression of liver fibrosis to cirrhosis. Taken together, these findings suggest that SNAP-23 is an important regular of actin dynamics in myofibroblastic HSC, but that the role of SNAP-23 in the progression of liver fibrosis in vivo is unclear.
MeSH term(s)	Actin Cytoskeleton/chemistry ; Actin Cytoskeleton/ultrastructure ; Actin Depolymerizing Factors/biosynthesis ; Actins/analysis ; Animals ; Carbon Tetrachloride/toxicity ; Cell Line ; Cell Movement ; Cell Separation ; Gene Knockdown Techniques ; Hepatic Stellate Cells/metabolism ; Hepatic Stellate Cells/ultrastructure ; Humans ; Liver/cytology ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/pathology ; Mice ; Myofibroblasts/ultrastructure ; Qb-SNARE Proteins/antagonists & inhibitors ; Qb-SNARE Proteins/deficiency ; Qb-SNARE Proteins/genetics ; Qb-SNARE Proteins/physiology ; Qc-SNARE Proteins/antagonists & inhibitors ; Qc-SNARE Proteins/deficiency ; Qc-SNARE Proteins/genetics ; Qc-SNARE Proteins/physiology ; RNA Interference ; RNA, Small Interfering/genetics ; RNA, Small Interfering/pharmacology ; Signal Transduction ; Stress Fibers/chemistry ; Stress Fibers/ultrastructure ; Wound Healing ; rho-Associated Kinases/physiology
Chemical Substances	Actin Depolymerizing Factors ; Actins ; Qb-SNARE Proteins ; Qc-SNARE Proteins ; RNA, Small Interfering ; SNAP23 protein, human ; Snap23 protein, mouse ; Carbon Tetrachloride (CL2T97X0V0) ; rho-Associated Kinases (EC 2.7.11.1)
Language	English
Publishing date	2019-11-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	1151108-4
ISSN	1555-3884 ; 1052-2116
ISSN (online)	1555-3884
ISSN	1052-2116
DOI	10.3727/105221619X15742818049365
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Zs.A 3683: Show issues

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Article ; Online: How does coffee prevent liver fibrosis? Biological plausibility for recent epidemiological observations.

Dranoff, Jonathan A / Feld, Jordan J / Lavoie, Elise G / Fausther, Michel

Hepatology (Baltimore, Md.)

2014 Volume 60, Issue 2, Page(s) 464–467

MeSH term(s)	Caffeine/therapeutic use ; Central Nervous System Stimulants/therapeutic use ; Coffee ; Humans ; Liver Cirrhosis/epidemiology ; Liver Cirrhosis/physiopathology ; Liver Cirrhosis/prevention & control ; Risk Factors ; Xanthines/therapeutic use
Chemical Substances	Central Nervous System Stimulants ; Coffee ; Xanthines ; Caffeine (3G6A5W338E)
Language	English
Publishing date	2014-05-27
Publishing country	United States
Document type	Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1002/hep.27032
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