2018
Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice
Hintermann E, Bayer M, Conti CB, Fuchs S, Fausther M, Leung PS, Aurrand-Lions M, Taubert R, Pfeilschifter JM, Friedrich-Rust M, Schuppan D, Dranoff JA, Gershwin ME, Manns MP, Imhof BA, Christen U. Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice. Journal Of Autoimmunity 2018, 91: 83-96. PMID: 29753567, DOI: 10.1016/j.jaut.2018.05.001.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell AdhesionCell Adhesion MoleculesCells, CulturedCholangitis, SclerosingDisease Models, AnimalEndothelial CellsFatty Acids, MonounsaturatedFemaleFibrosisHepatitis, AutoimmuneHumansImmunoglobulinsInflammationLiverLiver Cirrhosis, BiliaryMiceMice, Inbred C57BLMice, KnockoutMyocytes, Smooth MuscleMyofibroblastsVascular RemodelingVasoconstrictionConceptsPrimary sclerosing cholangitisHepatic stellate cellsPrimary biliary cholangitisPortal fibroblastsJunctional adhesion molecule JAMEndothelial cellsLiver fibrosisBile duct stricturesChronic liver diseaseAnti-fibrosis therapyBiopsies of patientsLoss of JAMRole of JAMSmooth muscle cellsEndothelial JAMIntrahepatic vasoconstrictionFunction of JAMSclerosing cholangitisDuct stricturesLiver inflammationBiliary cholangitisBiliary fibrosisChronic modelLeukocyte infiltrationLiver disease
2017
The Cholangiocyte Adenosine‐IL-6 Axis Regulates Survival During Biliary Cirrhosis
Lavoie EG, Fausther M, Goree JR, Dranoff JA. The Cholangiocyte Adenosine‐IL-6 Axis Regulates Survival During Biliary Cirrhosis. Gene Expression 2017, 17: 327-340. PMID: 28893353, PMCID: PMC5885153, DOI: 10.3727/105221617x15042723767876.Peer-Reviewed Original ResearchConceptsBile duct ligationIL-6 releaseExogenous IL-6Common bile duct ligationBiliary cirrhosisIL-6Duct ligationInjury responseIL-6 mRNA expressionIL-6 upregulationIL-6 secretionA2B adenosine receptorsLiver cell typesA2BAR activationBile infarctsInflammatory cellsCirrhosisEpithelial responseH69 cellsIntracellular Ca2Adenosine receptorsExtracellular adenosineInduces releaseMRNA expressionRegulates SurvivalAn Elf2-like transcription factor acts as repressor of the mouse ecto-5′-nucleotidase gene expression in hepatic myofibroblasts
Fausther M, Lavoie EG, Goree JR, Dranoff JA. An Elf2-like transcription factor acts as repressor of the mouse ecto-5′-nucleotidase gene expression in hepatic myofibroblasts. Purinergic Signalling 2017, 13: 417-428. PMID: 28667437, PMCID: PMC5714833, DOI: 10.1007/s11302-017-9570-7.Peer-Reviewed Original ResearchConceptsLiver myofibroblastsHepatic fibrosisChronic liver injuryNon-parenchymal liver cellsTissue repair processEffector cellsLiver injuryLiver fibrosisHepatic myofibroblastsMyofibroblast functionContractile propertiesPathological wound healingExtracellular adenosineMyofibroblastsImportant mediatorPromoter transcriptional activityFibrosisLiver cellsGene expressionWound healingEndogenous moleculesImportant regulatorHeterogeneous populationLocal microenvironmentFactor acts
2016
Sortilin Deficiency Reduces Ductular Reaction, Hepatocyte Apoptosis, and Liver Fibrosis in Cholestatic-Induced Liver Injury
Hubel E, Saroha A, Park WJ, Pewzner-Jung Y, Lavoie EG, Futerman AH, Bruck R, Fishman S, Dranoff JA, Shibolet O, Zvibel I. Sortilin Deficiency Reduces Ductular Reaction, Hepatocyte Apoptosis, and Liver Fibrosis in Cholestatic-Induced Liver Injury. American Journal Of Pathology 2016, 187: 122-133. PMID: 27842214, DOI: 10.1016/j.ajpath.2016.09.005.Peer-Reviewed Original ResearchConceptsBile duct ligationSerum IL-6IL-6Hepatocyte apoptosisWT miceLiver fibrosisCholangiocyte proliferationHepatic stellate cell activationCholestatic liver damageIL-6 neutralizationStellate cell activationHepatic stellate cellsASMase activityCarbon tetrachloride treatmentCarbon tetrachloride modelSortilin deficiencyHepatic inflammationLiver inflammationHepatocellular injuryLiver injuryLiver damageHepatic fibrosisBiliary damageDuctular reactionDuct ligation
2014
Pathological Changes in Pulmonary Circulation in Carbon Tetrachloride (ccl4)-Induced Cirrhotic Mice
Das M, Boerma M, Goree JR, Lavoie EG, Fausther M, Gubrij IB, Pangle AK, Johnson LG, Dranoff JA. Pathological Changes in Pulmonary Circulation in Carbon Tetrachloride (ccl4)-Induced Cirrhotic Mice. PLOS ONE 2014, 9: e96043. PMID: 24763616, PMCID: PMC3999097, DOI: 10.1371/journal.pone.0096043.Peer-Reviewed Original ResearchConceptsPulmonary acceleration timeCirrhotic micePortopulmonary hypertensionPulmonary circulationPathological changesSpleen weight/body weight ratioVentricle weight/body weightWeight/body weight ratioChronic CCl4 treatmentPulmonary vascular diseaseMale C57BL/6 miceBody weight ratioTimes/weekOxidative stress markersNovel therapeutic interventionsPicrosirius red stainingSterile olive oilPortal hypertensionEffects of CCl4Pulmonary arteryC57BL/6 micePathophysiological mechanismsPulmonary vasculaturePerivascular collagenVascular disease
2006
Adenosine inhibits cytosolic calcium signals and chemotaxis in hepatic stellate cells
Hashmi AZ, Hakim W, Kruglov EA, Watanabe A, Watkins W, Dranoff JA, Mehal WZ. Adenosine inhibits cytosolic calcium signals and chemotaxis in hepatic stellate cells. AJP Gastrointestinal And Liver Physiology 2006, 292: g395-g401. PMID: 17053161, PMCID: PMC3224076, DOI: 10.1152/ajpgi.00208.2006.Peer-Reviewed Original ResearchConceptsCytosolic Ca2Collagen I mRNATGF-beta productionHepatic stellate cell biologyLX-2 cellsEffects of adenosineHepatic stellate cellsSite of injuryI mRNAElevated tissue levelsDose-dependent mannerHigh adenosine concentrationsStellate cell biologyAdenylate cyclase inhibitorActivation markersLiver fibrosisTissue injuryHSC chemotaxisStellate cellsCyclase inhibitorAdenosine concentrationTranswell systemInhibited increasesCellular hypoxiaTissue levels