Search results for "hepatocytes"

showing 10 items of 224 documents

Targeted therapy of liver fibrosis/cirrhosis and its complications.

2011

Department of Pharmacokinetics, Toxicology, and Targeting, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands; Division of Gastroenterology and Hepatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA; Division of Molecular and Translational Medicine, Johannes Gutenberg University, Langenbeckstr. 1, 55131 Mainz, Germany

Liver Cirrhosismedicine.medical_specialtyCirrhosisMacrophageKupffer CellsLiver fibrosismedicine.medical_treatmentKupffer cellTargeted therapyMyoblastsDrug Delivery SystemsInternal medicinemedicineHepatic Stellate CellsHumansHepatocyteMolecular Targeted TherapyHCCMyofibroblastTargetingDrug CarriersHepatologybusiness.industryGeneral surgeryAntifibrotic therapyMedical schoolTranslational medicineHepatologyFibroblastsmedicine.diseaseFibrosisLiverStellate cellHepatocytesDrugbusinessCholangiocyteJournal of hepatology
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Competency of different cell models to predict human hepatotoxic drugs.

2014

The liver is the most important target for drug-induced toxicity. This vulnerability results from functional liver features and its role in the metabolic elimination of most drugs. Drug-induced liver injury is a significant leading cause of acute, chronic liver disease and an important safety issue when developing new drugs.This review describes the advantages and limitations of hepatic cell-based models for early safety risk assessment during drug development. These models include hepatocytes cultured as monolayer, collagen-sandwich; emerging complex 3D configuration; liver-derived cell lines; stem cell-derived hepatocytes.In vitro toxicity assays performed in hepatocytes or hepatoma cell …

Liver cytologyCellPharmacologyBiologyToxicologyBioinformaticsChronic liver diseaseCell LineCell Line TumorToxicity TestsmedicineAnimalsHumansCells CulturedPharmacologyLiver injuryGeneral Medicinemedicine.diseasemedicine.anatomical_structureDrug developmentLiverCell cultureToxicityHepatic stellate cellHepatocytesChemical and Drug Induced Liver InjuryExpert opinion on drug metabolismtoxicology
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Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use…

2013

This review encompasses the most important advances in liver functions and hepatotoxicity and analyzes which mechanisms can be studied in vitro. In a complex architecture of nested, zonated lobules, the liver consists of approximately 80 % hepatocytes and 20 % non-parenchymal cells, the latter being involved in a secondary phase that may dramatically aggravate the initial damage. Hepatotoxicity, as well as hepatic metabolism, is controlled by a set of nuclear receptors (including PXR, CAR, HNF-4α, FXR, LXR, SHP, VDR and PPAR) and signaling pathways. When isolating liver cells, some pathways are activated, e.g., the RAS/MEK/ERK pathway, whereas others are silenced (e.g. HNF-4α), resulting in…

MAPK/ERK pathwayHealth Toxicology and MutagenesisNF-KAPPA-BReceptors Cytoplasmic and NuclearReview ArticlePharmacologyToxicologyToxicogeneticsNon-parenchymal cells0302 clinical medicineInduced pluripotent stem cellANION-TRANSPORTING POLYPEPTIDECONSTITUTIVE ANDROSTANE RECEPTOR0303 health sciencesGeneral Medicine3. Good healthCell biologymedicine.anatomical_structureLiver030220 oncology & carcinogenesisHepatocyte[SDV.TOX]Life Sciences [q-bio]/ToxicologyInactivation MetabolicClearanceDILIStem cellPLURIPOTENT STEM-CELLSFARNESOID-X-RECEPTORSignal TransductionMechanisms of gene regulationARYL-HYDROCARBON RECEPTORCell signalingPharmacology and ToxicologyHEPATIC STELLATE CELLSBiology03 medical and health sciencesOrgan Culture TechniquesIn vivoCulture TechniquesToxicity TestsmedicineMathematical modeling.AnimalsHumansLiver X receptorDRUG-DRUG INTERACTIONS030304 developmental biologyCryopreservation[INFO.INFO-MO]Computer Science [cs]/Modeling and Simulation3D ModelsCoculture TechniquesHigh-Throughput Screening AssaysSALT EXPORT PUMPGene Expression RegulationHepatic stellate cellHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyPRIMARY RAT HEPATOCYTESMathematical modeling
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The role of death effector domain (DED)-containing proteins in acute oxidative cell injury in hepatocytes

2012

Abstract Apoptosis is a mechanism that regulates hepatic tissue homeostasis and contributes to both acute and chronic injury in liver disease. The apoptotic signaling cascade involves activation of the death-inducing signaling complex (DISC) and subsequent recruitment of proteins containing death effector domains (DED), which regulate downstream effector molecules. Prominent among these are the Fas-associated death domain (FADD) and the cellular caspase 8-like inhibitory protein (cFLIP), and alterations in these proteins can lead to severe disruption of physiological processes, including acute liver failure or hepatocellular carcinoma. Their role in cell signaling events independent of the …

MAPK/ERK pathwayProgrammed cell deathDeath Domain Receptor Signaling Adaptor ProteinsbiologyBlotting WesternBiochemistryArticleCell biologyMiceMicroscopy FluorescencePhysiology (medical)Cell Line TumorDeath-inducing signaling complexModels Animalbiology.proteinHepatocytesAnimalsHumansDeath effector domainFADDSignal transductionCaspaseDeath domainSignal Transduction
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Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Modulation of the hepatic fatty acid pool in peroxisomal 3-ketoacyl-CoA thiolase B-null mice exposed to the selective PPARalpha agonist Wy14,643

2009

10 pages; International audience; The peroxisomal 3-ketoacyl-CoA thiolase B (Thb) gene was previously identified as a direct target gene of PPARalpha, a nuclear hormone receptor activated by hypolipidemic fibrate drugs. To better understand the role of ThB in hepatic lipid metabolism in mice, Sv129 wild-type and Thb null mice were fed or not the selective PPARalpha agonist Wy14,643 (Wy). Here, it is shown that in contrast to some other mouse models deficient for peroxisomal enzymes, the hepatic PPARalpha signaling cascade in Thb null mice was normal under regular conditions. It is of interest that the hypotriglyceridemic action of Wy was reduced in Thb null mice underlining the conclusion t…

MESH : RNA MessengerMESH: Microsomes LiverMESH : PyrimidinesMono-unsaturated fatty acids n-7 and n-9MESH : Hepatocytes[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMESH: Mice KnockoutPPARαBiochemistryMESH: Acetyl-CoA C-AcetyltransferaseStearoyl-CoA desaturase-1MESH: HepatocytesMicechemistry.chemical_compoundMESH : Lipid MetabolismWy14MESH: AnimalsPeroxisomal 3-ketoacyl-CoA thiolase BAcetyl-CoA C-AcetyltransferaseMESH: PPAR alphaMESH : Fatty AcidsMESH: Lipid MetabolismMice Knockoutchemistry.chemical_classificationThiolaseFatty Acids643General MedicinePeroxisomeMESH : Stearoyl-CoA DesaturaseMESH: Fatty AcidsMESH : Microsomes LiverMESH : Acetyl-CoA C-AcetyltransferaseMicrosomes LiverMono-unsaturated fatty acids n-7 and n-9; Peroxisomal 3-ketoacyl-CoA thiolase B; PPARα; Stearoyl-CoA desaturase-1; Wy14643lipids (amino acids peptides and proteins)Stearoyl-CoA DesaturasePolyunsaturated fatty acidmedicine.medical_specialtyMESH : PPAR alphaMESH : Mice Inbred C57BL[ SDV.BBM.BM ] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyBiologyMESH: Mice Inbred C57BLInternal medicineMESH : MicePeroxisomesmedicineAnimalsHumansPPAR alphaRNA MessengerMESH: MiceMESH: RNA MessengerSCP2MESH: HumansMESH : HumansFatty acid[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyStearoyl-CoALipid MetabolismMESH: PeroxisomesSterol regulatory element-binding proteinMice Inbred C57BLPyrimidinesEndocrinologychemistryMESH: PyrimidinesMESH: Stearoyl-CoA DesaturaseHepatocytesMESH : Mice KnockoutMESH : AnimalsStearoyl-CoA desaturase-1MESH : PeroxisomesBiochimie
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Extra collagen overlay prolongs the differentiated phenotype in sandwich-cultured rat hepatocytes

2018

INTRODUCTION: Sandwich-cultured rat hepatocytes (SCRH) have become an invaluable in vitro model to study hepatic drug disposition. SCRH are maintained between two layers of extracellular matrix. In this configuration, culture periods of 4days are typically applicable. The aim of the present study was to modify conventional SCRH by applying an additional collagen overlay to prolong the hepatic phenotype in SCRH and thus to extend the applicability of the model. METHODS: The cultures receiving an extra top layer ('SCRH-plus' cultures) were compared with the conventional SCRH by testing the morphology, cell functionality, metabolic capacity and Mrp2-activity. RESULTS: In the SCRH-plus cultures…

Male0301 basic medicineGlucuronosyltransferaseCellular differentiationCellCell Culture TechniquesToxicologyExtracellular matrix03 medical and health sciencesBile canaliculiMethodsmedicineAnimalsBileGlucuronosyltransferaseRats WistarCells CulturedPharmacologybiologyCell DifferentiationMetabolismPhenotypeExtracellular MatrixRatsCell biologyPhenotype030104 developmental biologymedicine.anatomical_structureLiverBiochemistryCell cultureToxicityHepatocytesbiology.proteinHepatic drug dispositionCollagenSandwich-cultured hepatocytesJournal of Pharmacological and Toxicological Methods
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Direct conversion of human fibroblast to hepatocytes using a single inducible polycistronic vector

2019

Abstract Background Human fibroblasts can be reprogrammed into induced hepatocyte-like cells through the expression of a set of transcription factors. Although the generation of induced hepatocyte-like cells by HNF4A, HNF1A, and FOXA3 expression has proven to be a robust experimental strategy, using multiple lentivirus results in a highly variable heterogeneous population. Methods We designed and implemented a novel approach based on the delivery of reprogramming factors and green fluorescent protein in a single doxycycline-inducible lentiviral vector using 2A self-cleaving peptides. Results Fibroblasts infected with the lentiviral vector can be amplified in basic fibroblast culture media i…

Male0301 basic medicineInducibleGenetic VectorsGreen Fluorescent ProteinsMedicine (miscellaneous)Biochemistry Genetics and Molecular Biology (miscellaneous)Cell LineViral vectorGreen fluorescent proteinlcsh:BiochemistryMice03 medical and health sciences0302 clinical medicinePolycistronic vectorsmedicineAnimalsHumanslcsh:QD415-436TransgenesFibroblastGeneTranscription factorlcsh:R5-920ChemistryResearchReprogrammingDermisCell BiologyFibroblastsCellular ReprogrammingCell biologyInduced hepatocyte-like cellsiHEPPhenotype030104 developmental biologymedicine.anatomical_structureGenes030220 oncology & carcinogenesisDoxycyclineHepatocytesMolecular MedicineFOXA3Stem celllcsh:Medicine (General)ReprogrammingStem Cell Research & Therapy
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Both cholestatic and steatotic drugs trigger extensive alterations in the mRNA level of biliary transporters in rat hepatocytes: Application to devel…

2016

Disruption of the vectorial bile acid transport in the liver is a key feature of cholestatic drugs, although many causal and mechanistic aspects are still unknown. The aim of the present study was to explore if cholestatic drugs can repress or induce the expression of hepatic transporters. To this end, sandwich-cultured rat hepatocytes were treated with cholestatic and non-cholestatic (steatotic, non-hepatotoxic, etc.) drugs and the mRNA expression of 10 uptake and efflux biliary transporters was measured. Results evidenced that all cholestatic drugs cause extensive alterations in the mRNA expression of most biliary transporters. Surprisingly, nearly all steatotic drugs also affected the ex…

Male0301 basic medicinePathologymedicine.medical_specialtyDrug-Related Side Effects and Adverse ReactionsDrug Evaluation PreclinicalOrganic Anion Transporters Sodium-IndependentPharmacologyBiologyToxicology030226 pharmacology & pharmacyRats Sprague-Dawley03 medical and health sciences0302 clinical medicineCholestasisPredictive Value of TestsIn vivomedicineAnimalsBileRNA MessengerCells CulturedCholestasisMultidrug resistance-associated protein 2Fatty liverTransporterGeneral Medicinemedicine.diseaseRatsFatty Liver030104 developmental biologyTetracyclinesHepatocytesBiomarker (medicine)EffluxSteatosisCarrier ProteinsBiomarkersToxicology Letters
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