2024
Gly-β-MCA is a potent anti-cholestasis agent against “human-like” hydrophobic bile acid-induced biliary injury in mice
Hasan M, Wang H, Luo W, Clayton Y, Gu L, Du Y, Palle S, Chen J, Li T. Gly-β-MCA is a potent anti-cholestasis agent against “human-like” hydrophobic bile acid-induced biliary injury in mice. Journal Of Lipid Research 2024, 65: 100649. PMID: 39306039, PMCID: PMC11526081, DOI: 10.1016/j.jlr.2024.100649.Peer-Reviewed Original ResearchUrsodeoxycholic acid treatmentUrsodeoxycholic acidPortal fibrosisHepatobiliary injuryClinically relevant dosesMuricholic acidsChronic liver diseaseBile acidsEndogenous bile acidsHydrophobic bile acidsPortal inflammationBile acid pool compositionLithocholic acidTherapeutic optionsBiliary injuryKO miceLine drugsBile acid pool sizeSerum transaminasesBile acid poolRelevant dosesDuctular reactionLiver diseaseCholestasisCholestasis modelPortal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities
Gupta V, Sehrawat T, Pinzani M, Strazzabosco M. Portal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities. Gastroenterology 2024, 168: 675-690. PMID: 39251168, PMCID: PMC11885590, DOI: 10.1053/j.gastro.2024.07.044.Peer-Reviewed Original ResearchLiver diseasePortal fibrosisDuctular reactionPathological repairProgression of liver diseaseCholestatic liver diseaseTranslational opportunitiesChronic liver diseaseProgression of fibrosisCell typesChronic human liver diseaseHuman liver diseaseTumor microenvironmentTherapeutic advancesImmune modulationHistological abnormalitiesVascular changesLiver repairPathophysiological roleFibrosisTreatment prospectsPortal spacesMesenchymal cellsVascular cellsComplex crosstalk
2023
Focal nodular hyperplasia–like nodules arising in the setting of hepatic vascular disorders with portosystemic shunting show β-catenin activation
Umetsu S, Joseph N, Cho S, Morotti R, Deshpande V, Jain D, Kakar S. Focal nodular hyperplasia–like nodules arising in the setting of hepatic vascular disorders with portosystemic shunting show β-catenin activation. Human Pathology 2023, 142: 20-26. PMID: 37806391, DOI: 10.1016/j.humpath.2023.09.010.Peer-Reviewed Original ResearchConceptsHepatic vascular disordersFocal nodular hyperplasiaFNH-like nodulesHepatocellular adenomaVascular disordersHepatocellular carcinomaΒ-catenin activationPortosystemic shuntRegenerative nodulesFocal nodular hyperplasia-like nodulesPost-Fontan procedureGlutamine synthetase stainingAbernethy malformationLiver resectionPortosystemic shuntingHistologic featuresMalignant neoplasmsNodular lesionsVascular diseaseDuctular reactionNodular hyperplasiaNodular architectureHepatocellular nodulesBenign lesionsFibrous septaCombining ASBT inhibitor and FGF15 treatments enhances therapeutic efficacy against cholangiopathy in female but not male Cyp2c70 KO mice
Hasan M, Chen J, Matye D, Wang H, Luo W, Gu L, Clayton Y, Du Y, Li T. Combining ASBT inhibitor and FGF15 treatments enhances therapeutic efficacy against cholangiopathy in female but not male Cyp2c70 KO mice. Journal Of Lipid Research 2023, 64: 100340. PMID: 36737039, PMCID: PMC9986646, DOI: 10.1016/j.jlr.2023.100340.Peer-Reviewed Original ResearchConceptsBile acid poolKO miceTherapeutic efficacyHepatobiliary injuryBile acid pool sizeBile acid exposureGut barrier integrityGut barrier functionBile acid metabolismAcid poolBile acid synthesisAcid pool sizeBile acid uptakePortal inflammationPortal fibrosisGut exposureDuctular reactionGSK2330672Therapeutic reductionUrsodeoxycholic acidMuricholic acidAcid exposureASBT inhibitorSevere cholangiopathyBarrier integrity
2022
Clinical, histological and molecular profiling of different stages of alcohol-related liver disease
Ventura-Cots M, Argemi J, Jones PD, Lackner C, Hag M, Abraldes JG, Alvarado E, Clemente A, Ravi S, Alves A, Alboraie M, Altamirano J, Barace S, Bosques F, Brown R, Caballeria J, Cabezas J, Carvalhana S, Cortez-Pinto H, Costa A, Degré D, Fernandez-Carrillo C, Ganne-Carrie N, Garcia-Tsao G, Genesca J, Koskinas J, Lanthier N, Louvet A, Lozano JJ, Lucey MR, Masson S, Mathurin P, Mendez-Sanchez N, Miquel R, Moreno C, Mounajjed T, Odena G, Kim W, Sancho-Bru P, Sands R, Szafranska J, Verset L, Schnabl B, Sempoux C, Shah V, Shawcross DL, Stauber RE, Straub BK, Verna E, Tiniakos D, Trépo E, Vargas V, Villanueva C, Woosley JT, Ziol M, Mueller S, Stärkel P, Bataller R. Clinical, histological and molecular profiling of different stages of alcohol-related liver disease. Gut 2022, 71: 1856-1866. PMID: 34992134, PMCID: PMC11034788, DOI: 10.1136/gutjnl-2021-324295.Peer-Reviewed Original ResearchConceptsAlcohol-related liver diseaseAlcohol-related hepatitisAH patientsLiver diseaseAlcohol intakeDuctular reactionGamma-glutamyl transferase levelsProfound liver failureSevere neutrophil infiltrationWorse liver functionObservational multicentre studyOne-year mortalityBile acid metabolismMallory-Denk bodiesRNA microarray analysisNeutrophil infiltrationProspective cohortRetrospective cohortAdvanced fibrosisLiver failureMulticentre studySteatosis gradeLiver functionPericellular fibrosisSevere fibrosis
2021
Long non-coding RNA ACTA2-AS1 promotes ductular reaction by interacting with the p300/ELK1 complex
Navarro-Corcuera A, Sehrawat T, Jalan-Sakrikar N, Gibbons H, Pirius N, Khanal S, Hamdan F, Aseem S, Cao S, Banales J, Kang N, Faubion W, LaRusso N, Shah V, Huebert R. Long non-coding RNA ACTA2-AS1 promotes ductular reaction by interacting with the p300/ELK1 complex. Journal Of Hepatology 2021, 76: 921-933. PMID: 34953958, PMCID: PMC8934273, DOI: 10.1016/j.jhep.2021.12.014.Peer-Reviewed Original ResearchConceptsBile duct ligationDuctular reactionACTA2-AS1KO miceBile duct cellsLPS exposureBiliary diseaseFibrogenic markersInjury modelDuct ligationFibrogenic genesLong non-coding RNAsFl/Cholangiocyte proliferationFibrosisHuman cholangiocytesSGC-CBP30Primary cholangiocytesAbstractTextLiver tissueLAY SUMMARYP300 inhibitorTranscription factorsCholangiocytesDuct cellsThe Neglected Role of Bile Duct Epithelial Cells in NASH
Cadamuro M, Lasagni A, Sarcognato S, Guido M, Fabris R, Strazzabosco M, Strain AJ, Simioni P, Villa E, Fabris L. The Neglected Role of Bile Duct Epithelial Cells in NASH. Seminars In Liver Disease 2021, 42: 034-047. PMID: 34794182, DOI: 10.1055/s-0041-1739455.Peer-Reviewed Original ResearchConceptsNonalcoholic fatty liver diseaseNonalcoholic steatohepatitisLiver diseaseInsulin resistancePrevalent liver diseaseBile duct epithelial cellsFatty liver diseaseSubset of patientsCommon pathogenetic mechanismDuct epithelial cellsMultiple biological effectsFibro-inflammationHepatic manifestationNAFLD patientsPortal fibrosisMetabolic syndromeBile ductDuctular reactionDisease progressionPathogenetic mechanismsLiver cancerMetabolic alterationsProgenitor cell compartmentEpithelial cellsDiseaseLiver Pathology, Including MOC31 Immunohistochemistry, in Congenital Tufting Enteropathy
Chen S, Goldsmith J, Fawaz R, Al-Ibraheemi A, Perez-Atayde A, Vargas S. Liver Pathology, Including MOC31 Immunohistochemistry, in Congenital Tufting Enteropathy. The American Journal Of Surgical Pathology 2021, 45: 1091-1097. PMID: 33756496, DOI: 10.1097/pas.0000000000001710.Peer-Reviewed Original ResearchConceptsCTE patientsCongenital tufting enteropathyParenteral nutritionBiliary epitheliumDuctular reactionLiver pathologyChronic hepatitis CHepatitis C patientsEpithelial cell adhesion moleculeLiver core biopsyIntestinal villous atrophyNormal brush borderClinicopathologic materialEpCAM-deficientCore biopsyTufting enteropathyC patientsEpCAM mutationsCell adhesion moleculesHepatitis CLiver biopsyMOC31Affected patientsLobular inflammationPathological findings
2020
Liver Matrix in Benign and Malignant Biliary Tract Disease
Fabris L, Cadamuro M, Cagnin S, Strazzabosco M, Gores G. Liver Matrix in Benign and Malignant Biliary Tract Disease. Seminars In Liver Disease 2020, 40: 282-297. PMID: 32162285, DOI: 10.1055/s-0040-1705109.Peer-Reviewed Original ResearchConceptsMalignant biliary tract diseasesBiliary tract diseaseExtracellular matrixReactive ductular cellsPro-oncogenic effectsHepatic progenitor cellsExtracellular matrix undergoesBiliary repairDuctular reactionTract diseaseBiliary damageMalignant transformationResident cellsDuctular cellsMain molecular factorsProgenitor cellsMolecular factorsMechanical signalsLiver matrixNoncollagenous glycoproteinsStructural alterationsDirect interactionBiochemical compositionCellsMultifunctional molecules
2017
Notch signaling and progenitor/ductular reaction in steatohepatitis
Morell CM, Fiorotto R, Meroni M, Raizner A, Torsello B, Cadamuro M, Spagnuolo G, Kaffe E, Sutti S, Albano E, Strazzabosco M. Notch signaling and progenitor/ductular reaction in steatohepatitis. PLOS ONE 2017, 12: e0187384. PMID: 29140985, PMCID: PMC5687773, DOI: 10.1371/journal.pone.0187384.Peer-Reviewed Original ResearchConceptsHepatic stellate cellsDuctular reactionRole of NotchMCD diet-fed miceMethionine-choline deficient (MCD) dietHepatic progenitor cell activationPrimary hepatic stellate cellsChronic liver diseaseDiet-fed miceTGF-β1 expressionAlternative therapeutic targetsTGF-β1 treatmentProgenitor cell activationNotch-1 activationLiver injuryMCD dietLiver diseaseFibrosis progressionNotch signalingDR responseLiver repairBSEP expressionHepatocyte cell lineLiver cancerAAV8-TBGAnimal models of biliary injury and altered bile acid metabolism
Mariotti V, Strazzabosco M, Fabris L, Calvisi DF. Animal models of biliary injury and altered bile acid metabolism. Biochimica Et Biophysica Acta (BBA) - Molecular Basis Of Disease 2017, 1864: 1254-1261. PMID: 28709963, PMCID: PMC5764833, DOI: 10.1016/j.bbadis.2017.06.027.Peer-Reviewed Original ResearchConceptsBile acid metabolismBiliary injuryMouse modelAnimal modelsDistinct immune systemCholestatic liver injuryAcid metabolismJesus BanalesMarco MarzioniNicholas LaRussoPeter JansenBiliary repairLiver injuryDuctular reactionLiver repairObstructive cholestasisDisease progressionPeribiliary inflammationMain phenotypic featuresBiliary dysgenesisViral infectionImmune systemLiver homeostasisLiver phenotypeHuman setting
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 ligationThe Spectrum of Histologic Findings in Hepatic Outflow Obstruction
Gonzalez RS, Gilger MA, Huh WJ, Washington MK. The Spectrum of Histologic Findings in Hepatic Outflow Obstruction. Archives Of Pathology & Laboratory Medicine 2016, 141: 98-103. PMID: 27681331, PMCID: PMC6420777, DOI: 10.5858/arpa.2015-0388-oa.Peer-Reviewed Original ResearchConceptsHepatic outflow obstructionPortal tract changesCardiac hepatopathyBudd-Chiari syndromeOutflow obstructionHistologic findingsBudd-ChiariSinusoidal fibrosisSinusoidal dilationTract changesCentral veinHepatic venous outflow obstructionVenous outflow obstructionBile ductular reactionDistinctive histologic findingsHepatocyte dropoutDifferent pathophysiologyPrior diagnosisChronic inflammationCentrilobular necrosisDuctular reactionMorphologic findingsUndiagnosed patientsChronic natureHepatopathyDuctular reactions in the liver regeneration process with local inflammation after physical partial hepatectomy
Suzuki Y, Katagiri H, Wang T, Kakisaka K, Kume K, Nishizuka SS, Takikawa Y. Ductular reactions in the liver regeneration process with local inflammation after physical partial hepatectomy. Laboratory Investigation 2016, 96: 1211-1222. PMID: 27617400, DOI: 10.1038/labinvest.2016.97.Peer-Reviewed Original ResearchConceptsLiver regeneration processDuctular reactionMurine liver injury modelsLocal inflammatory responseLiver injury modelExtracellular matrix-associated genesPartial hepatectomy modelMatrix-associated genesStem/progenitor cellsLiver stem/progenitor cellsTissue repair processLiver regeneration studiesSystematic remodelingExtracellular matrix remodelingLeft lobeInflammatory cytokinesLocal inflammationLiver weightHepatocyte hypertrophyInflammatory responseInjury modelLocal injuryKi67 stainingSurgical proceduresEntire liverRevisiting Epithelial‐to‐Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the “Reactive” Biliary Epithelial Phenotype
Fabris L, Brivio S, Cadamuro M, Strazzabosco M. Revisiting Epithelial‐to‐Mesenchymal Transition in Liver Fibrosis: Clues for a Better Understanding of the “Reactive” Biliary Epithelial Phenotype. Stem Cells International 2016, 2016: 2953727. PMID: 26880950, PMCID: PMC4736590, DOI: 10.1155/2016/2953727.Peer-Reviewed Original ResearchDuctular reactive cellsDuctular reactionHepatic progenitor cell compartmentMesenchymal transitionBiliary epithelial phenotypeChronic biliary damageSevere hepatic disordersBile duct epithelial cellsEpithelial cellsLiver disease progressionDuct epithelial cellsNew antifibrotic therapiesPortal fibrosisInflammatory cellsLiver fibrosisAntifibrotic therapyBiliary damageDisease progressionHepatic disordersEMT changesReactive cellsMesenchymal markersHepatic scarringProgenitor cell compartmentCholangiopathy
2015
Connective tissue growth factor and integrin αvβ6: A new pair of regulators critical for ductular reaction and biliary fibrosis in mice
Pi L, Robinson P, Jorgensen M, Oh S, Brown A, Weinreb P, Le Trinh T, Yianni P, Liu C, Leask A, Violette S, Scott E, Schultz G, Petersen B. Connective tissue growth factor and integrin αvβ6: A new pair of regulators critical for ductular reaction and biliary fibrosis in mice. Hepatology 2015, 61: 678-691. PMID: 25203810, PMCID: PMC4303530, DOI: 10.1002/hep.27425.Peer-Reviewed Original ResearchMeSH KeywordsAdult Stem CellsAnimalsAntigens, NeoplasmBile Duct NeoplasmsBile Ducts, IntrahepaticCell AdhesionChemical and Drug Induced Liver InjuryCholangiocarcinomaConnective Tissue Growth FactorFemaleFibronectinsHumansIntegrinsLiver CirrhosisMaleMiceMice, KnockoutPyridinesRabbitsRatsTransforming Growth Factor beta1ConceptsConnective tissue growth factorDuctular reactionTissue growth factorIntegrin αvβ6Oval cell activationLiver injuryGrowth factorTamoxifen-inducible Cre-loxP systemCell activationRole of CTGFAlpha-smooth muscle actin stainingRelated liver diseasesSevere liver injuryGreen fluorescent protein reporter miceFibrosis-related genesMuscle actin stainingSirius red stainingPotential therapeutic targetHuman cirrhotic liversEpithelial cell adhesion moleculeDuctular epithelial cellsBiliary fibrosisCre-loxP systemLiver diseaseSerum markers
2014
Osteopontin: a new player in regulating hepatic ductular reaction and hepatic progenitor cell responses during chronic liver injury
Strazzabosco M, Fabris L, Albano E. Osteopontin: a new player in regulating hepatic ductular reaction and hepatic progenitor cell responses during chronic liver injury. Gut 2014, 63: 1693-1694. PMID: 25056656, PMCID: PMC4519840, DOI: 10.1136/gutjnl-2014-307712.Peer-Reviewed Original Research
2013
Diagnostic utility and limitations of glutamine synthetase and serum amyloid-associated protein immunohistochemistry in the distinction of focal nodular hyperplasia and inflammatory hepatocellular adenoma
Joseph NM, Ferrell LD, Jain D, Torbenson MS, Wu TT, Yeh MM, Kakar S. Diagnostic utility and limitations of glutamine synthetase and serum amyloid-associated protein immunohistochemistry in the distinction of focal nodular hyperplasia and inflammatory hepatocellular adenoma. Modern Pathology 2013, 27: 62-72. PMID: 23807780, DOI: 10.1038/modpathol.2013.114.Peer-Reviewed Original ResearchMeSH KeywordsAdenoma, Liver CellAdolescentAdultAgedBiomarkers, TumorBiopsyC-Reactive ProteinChildChild, PreschoolDiagnosis, DifferentialDiagnostic ErrorsFemaleFocal Nodular HyperplasiaGlutamate-Ammonia LigaseHumansImmunohistochemistryInflammation MediatorsLiver NeoplasmsMaleMiddle AgedPredictive Value of TestsSerum Amyloid A ProteinYoung AdultConceptsSerum amyloid-associated proteinFocal nodular hyperplasiaAmyloid-associated proteinsInflammatory hepatocellular adenomaNodular hyperplasiaHepatocellular adenomaStaining patternDuctular reactionFibrous stromaFocal nodular hyperplasia casesMap-like patternOverlapping histological featuresGlutamine synthetase stainingHistological featuresProtein immunohistochemistryHyperplasia casesIndeterminate lesionsPositive stainingHyperplasiaDiagnostic utilityAdenomasBlood vesselsFrequent overlapStainingDiagnostic errorsNotch signaling regulates tubular morphogenesis during repair from biliary damage in mice
Fiorotto R, Raizner A, Morell CM, Torsello B, Scirpo R, Fabris L, Spirli C, Strazzabosco M. Notch signaling regulates tubular morphogenesis during repair from biliary damage in mice. Journal Of Hepatology 2013, 59: 124-130. PMID: 23500150, PMCID: PMC3777645, DOI: 10.1016/j.jhep.2013.02.025.Peer-Reviewed Original ResearchMeSH Keywords1-NaphthylisothiocyanateAmyloid Precursor Protein SecretasesAnimalsBile Ducts, IntrahepaticCalcium-Binding ProteinsImmunoglobulin J Recombination Signal Sequence-Binding ProteinIntercellular Signaling Peptides and ProteinsJagged-1 ProteinLiver RegenerationMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMorphogenesisPyridinesReceptor, Notch2RNA, Small InterferingSerrate-Jagged ProteinsSignal TransductionStem CellsConceptsWild-type miceHepatic progenitor cellsBiliary damageType miceProgenitor cellsDuctular reactionΓ-secretase inhibitor treatmentTubule formationNotch signalingNotch-2 receptorRBP-JkBiliary repairMature ductsLiver-specific defectCKO miceInhibitor treatmentAbstractTextMiceNotch inhibitionNotch-1Jagged-1Notch-2ANITAIMSSOX-9
2012
Development of the bile ducts: Essentials for the clinical hepatologist
Strazzabosco M, Fabris L. Development of the bile ducts: Essentials for the clinical hepatologist. Journal Of Hepatology 2012, 56: 1159-1170. PMID: 22245898, PMCID: PMC3328609, DOI: 10.1016/j.jhep.2011.09.022.Peer-Reviewed Original ResearchConceptsLiver diseaseBile ductBiliary structuresFibropolycystic liver diseaseExtrahepatic biliary treeBiliary developmentLiver repair mechanismsHepatocellular damageBiliary treeDuctular reactionLiver repairReparative responseAlagille syndromePathogenic aspectsClinical hepatologistsCholangiopathyGrowth factorParacrine signalsEmbryonic lifeDiseaseDuctRepair mechanismsHepatologistsSyndromeTranscription factors
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