2015
Nuclear Factor, Erythroid 2-Like 2 Regulates Expression of Type 3 Inositol 1,4,5-Trisphosphate Receptor and Calcium Signaling in Cholangiocytes
Weerachayaphorn J, Amaya MJ, Spirli C, Chansela P, Mitchell-Richards KA, Ananthanarayanan M, Nathanson MH. Nuclear Factor, Erythroid 2-Like 2 Regulates Expression of Type 3 Inositol 1,4,5-Trisphosphate Receptor and Calcium Signaling in Cholangiocytes. Gastroenterology 2015, 149: 211-222.e10. PMID: 25796361, PMCID: PMC4478166, DOI: 10.1053/j.gastro.2015.03.014.Peer-Reviewed Original ResearchConceptsBile ductBile duct unitsCholestatic disordersOxidative stressCalcium signalingNuclear factorMouse cholangiocytesDuct unitsReduced calcium signalingIntrahepatic bile ductsLevels of Nrf2Cholangiocyte cellsKnockdown of Nrf2Activation of Nrf2Intracellular calcium release channelsTranscription factor Nrf2Binding of Nrf2Calcium release channelPolymerase chain reaction analysisBiliary diseaseTrisphosphate receptorControl ratsLiver disordersBicarbonate secretionChain reaction analysis
2013
Pediatric Cholestatic Disorders Approach to Pathologic Diagnosis
Morotti RA, Jain D. Pediatric Cholestatic Disorders Approach to Pathologic Diagnosis. Surgical Pathology Clinics 2013, 6: 205-225. PMID: 26838972, DOI: 10.1016/j.path.2013.03.001.Peer-Reviewed Original ResearchLiver diseaseDiagnostic challengePediatric cholestatic disordersClinical featuresPediatric groupHistopathologic featuresCholestatic disordersHistopathologic findingsPathologic diagnosisDifferential diagnosisDiagnostic modalitiesBile synthesisMolecular abnormalitiesDiagnosisDiseaseDisordersSignificant overlapPathophysiologyMolecular geneticsAbnormalities
2010
Cholestasis: Genetic and Acquired
Boyer J. Cholestasis: Genetic and Acquired. Seminars In Liver Disease 2010, 30: 113-115. PMID: 20422493, DOI: 10.1055/s-0030-1253220.Peer-Reviewed Original ResearchConceptsBile salt export pumpCholestatic liver diseaseMultidrug resistance protein 3Cholestatic liver injuryLiver diseaseBile acidsBile salt transportersIssue of SeminarsLiver injuryCholestatic disordersBile flowSulfate conjugatesSodium taurocholate co-transporting polypeptideBile duct-cannulated animalsBile formationExport pumpProtein 3Bile acid-independent bile flowSalt transportersTaurocholate co-transporting polypeptideOrganic solute transporters alphaDependent bile salt transporterApical sodium-dependent bile salt transporterFamilial intrahepatic cholestasis-1Drug-induced cholestasisThe Bile Salt Export Pump: Clinical and Experimental Aspects of Genetic and Acquired Cholestatic Liver Disease
Lam P, Soroka C, Boyer J. The Bile Salt Export Pump: Clinical and Experimental Aspects of Genetic and Acquired Cholestatic Liver Disease. Seminars In Liver Disease 2010, 30: 125-133. PMID: 20422495, PMCID: PMC3008346, DOI: 10.1055/s-0030-1253222.Peer-Reviewed Original ResearchConceptsBenign recurrent intrahepatic cholestasis type 2Progressive familial intrahepatic cholestasis type 2Bile salt export pumpDrug-induced cholestasisType 2Export pumpCholestatic liver diseaseBile salt secretionForms of cholestasisDifferent genetic formsLiver diseaseCholestatic disordersIntrahepatic cholestasisBSEP expressionPathophysiologic processesBSEP deficiencyAnimal modelsCholestasisGenetic formsBile saltsSalt secretionMolecular characteristicsPivotal roleCell culturesPrimary transporter
2001
Proinflammatory Cytokines Inhibit Secretion in Rat Bile Duct Epithelium
Spirlı̀ C, Nathanson M, Fiorotto R, Duner E, Denson L, Sanz J, Di Virgilio F, Okolicsanyi L, Casagrande F, Strazzabosco M. Proinflammatory Cytokines Inhibit Secretion in Rat Bile Duct Epithelium. Gastroenterology 2001, 121: 156-169. PMID: 11438505, DOI: 10.1053/gast.2001.25516.Peer-Reviewed Original ResearchConceptsProinflammatory cytokinesFluorescein-labeled dextranIL-1Interferon gammaCAMP-dependent fluid secretionCystic fibrosis transmembrane conductance regulatorBile duct epitheliumRat bile duct epitheliaTumor necrosis factorCyclic adenosine monophosphate levelsSecretin receptorAdenosine monophosphate levelsBile duct unitsDuctular cholestasisPortal inflammationCholestatic disordersIL-6Inflammatory cytokinesTNF-alphaBiliary epitheliumNecrosis factorCellular cyclic adenosine monophosphate (cAMP) levelsDuct epitheliumPurinergic agonistsSR expression
2000
Pathophysiology of the intrahepatic biliary epithelium
Strazzabosco M, Spirlì C, Okolicsanyi L. Pathophysiology of the intrahepatic biliary epithelium. Journal Of Gastroenterology And Hepatology 2000, 15: 244-253. PMID: 10764023, DOI: 10.1046/j.1440-1746.2000.02091.x.Peer-Reviewed Original ResearchConceptsIntrahepatic biliary epitheliumBiliary epitheliumIntrahepatic bile duct epitheliumChronic cholestatic disorderBile duct epitheliumCholangiocyte functionBasic disease mechanismsPortal inflammationBiliary atresiaGastrointestinal hormonesCholestatic disordersPathophysiological pointBiliary treeCholangiocyte pathophysiologyImmune regulationPharmacological approachesNormal epitheliumCholangiocyte proliferationCholangiopathyDuct epitheliumInfectious agentsImportant causeBile acidsCystic fibrosisImmunoglobulin A.
1999
Neonatal Cholestasis: A Red Alert for the Jaundiced Newborn
Pashankar D, Schreiber R. Neonatal Cholestasis: A Red Alert for the Jaundiced Newborn. Canadian Journal Of Gastroenterology And Hepatology 1999, 14: 67d-72d. PMID: 11110615, DOI: 10.1155/2000/657368.Peer-Reviewed Original ResearchConceptsNeonatal cholestasisNeonatal cholestatic disordersBile acid metabolismPersistent jaundiceYounger patientsPrompt diagnosisCholestatic disordersBile flowNeonatal jaundiceConjugated hyperbilirubinemiaJaundiced newbornsCholestasisTherapeutic interventionsEarly interventionAcid metabolismJaundiceHyperbilirubinemiaNewbornsFurther investigationInterventionPatientsPrognosisEtiopathogenesisInfantsRed alert
1998
Stimulation of bile duct epithelial secretion by glybenclamide in normal and cholestatic rat liver.
Nathanson MH, Burgstahler AD, Mennone A, Dranoff JA, Rios-Velez L. Stimulation of bile duct epithelial secretion by glybenclamide in normal and cholestatic rat liver. Journal Of Clinical Investigation 1998, 101: 2665-2676. PMID: 9637700, PMCID: PMC508857, DOI: 10.1172/jci2835.Peer-Reviewed Original ResearchConceptsBile duct epitheliumBicarbonate excretionBile flowDuct epitheliumImportant new therapeutic targetStimulatory effectBile duct segmentsBile duct cellsRat liverNew therapeutic targetsCardinal complicationLiver diseaseCholestatic disordersSecond messenger systemsCholestatic rat liverTherapeutic targetMeasurement of cAMPGlybenclamideEpithelial secretionDuct cellsDuct segmentsHepatocyte coupletsLiverExcretionEpithelium
1997
Transport systems in cholangiocytes: their role in bile formation and cholestasis.
Strazzabosco M. Transport systems in cholangiocytes: their role in bile formation and cholestasis. The Yale Journal Of Biology And Medicine 1997, 70: 427-34. PMID: 9626763, PMCID: PMC2589334.Peer-Reviewed Original ResearchConceptsBiliary epitheliumCa-activated Cl channelsChronic cholestatic disorderPathogenesis of cholestasisBile duct diseaseCholangiocyte deathFormation of bilePortal inflammationBiliary cirrhosisProinflammatory mediatorsLiver diseaseClinical picturePathophysiological pointCholestatic disordersDuct diseaseProliferative responseBiliary constituentsBile acidsCystic fibrosisPortal spacesSecretory functionBile formationCholestasisDuctular secretionSecretory activity
1993
Effects of tauroursodeoxycholic acid on cytosolic Ca2+ signals in isolated rat hepatocytes
Beuers U, Nathanson M, Boyer J. Effects of tauroursodeoxycholic acid on cytosolic Ca2+ signals in isolated rat hepatocytes. Gastroenterology 1993, 104: 604-612. PMID: 8425704, DOI: 10.1016/0016-5085(93)90433-d.Peer-Reviewed Original ResearchConceptsEffect of TUDCATauroursodeoxycholic acidAdministration of TUDCAIP3-independent mechanismCytosolic free calciumIP3-sensitive Ca2Trihydroxy bile acidsCholestatic disordersHepatocyte secretionTreatment periodExtracellular Ca2Bile acidsTaurolithocholic acidMumol/Rat hepatocytesFree calciumBasal levelsTransient increaseCytosolic Ca2Levels of inositolFree mediumPhysiological concentrationsIsolated rat hepatocytesHepatocytesFourfold increase
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