Search results for "hepatocyte"

showing 10 items of 369 documents

Hepatocellular expression of a dominant-negative mutant TGF-β type II receptor accelerates chemically induced hepatocarcinogenesis

2001

The potent growth-inhibitory activity of cytokines of the transforming growth factor-beta (TGF-beta) superfamily and their widespread expression in epithelia suggest that they may play an important role in the maintenance of epithelial homeostasis. To analyse TGF-beta mediated tumor suppressor activity in the liver, we generated transgenic mice overexpressing a dominant negative type II TGF-beta receptor in hepatocytes under control of the regulatory elements of the human C-reactive protein gene promoter. Transgenic animals exhibited constitutive and liver-specific transgene expression. The functional inactivation of the TGF-beta signaling pathway in transgenic hepatocytes was shown by redu…

MaleGenetically modified mouseCancer Researchmedicine.medical_specialtyCarcinoma HepatocellularTransgeneMice TransgenicProtein Serine-Threonine KinasesBiologymedicine.disease_causeMiceLiver Neoplasms ExperimentalTransforming Growth Factor betaInternal medicineGeneticsmedicineAnimalsRNA MessengerMolecular BiologyCells CulturedTissue homeostasisDNA synthesisReceptor Transforming Growth Factor-beta Type IICell biologyC-Reactive ProteinEndocrinologymedicine.anatomical_structureHepatocyteMutationHepatocytesSignal transductionCarcinogenesisReceptors Transforming Growth Factor betaTransforming growth factorOncogene
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Role of caspase-8 in hepatocyte response to infection and injury in mice.

2007

Caspase-8 has been implicated in signaling for apoptotic cell death and for certain nonapoptotic functions. However, knowledge of actual physiological or pathophysiological processes to which this enzyme contributes is lacking. Using a mouse model and employing the conditional knockout approach to delete the caspase-8 gene specifically in the liver, we found that caspase-8 deficiency in hepatocytes facilitates infection of the liver by Listeria monocytogenes, attenuates the hepatocyte proliferation wave during the first 48 hours after partial hepatectomy and, depending on the genetic background of the mice, prompts a chronic inflammatory response to the hepatectomy, as a result of which the…

Programmed cell deathInflammationCaspase 8MiceConditional gene knockoutmedicineAnimalsListeriosisCaspaseCell ProliferationInflammationMice KnockoutCaspase 8HepatologybiologyCell DeathCell growthLiver Regenerationmedicine.anatomical_structureHepatocyteImmunologyCancer researchChronic inflammatory responsebiology.proteinHepatocytesmedicine.symptomHepatology (Baltimore, Md.)
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Less but better: cardioprotective lipid profile of patients with GCK-MODY despite lower HDL cholesterol level

2014

Patients with diabetes caused by single-gene mutations generally exhibit an altered course of diabetes. Those with mutations of the glucokinase gene (GCK-MODY) show good metabolic control and low risk of cardiovascular complications despite paradoxically lowered high-density lipoprotein (HDL) cholesterol levels. In order to investigate the matter, we analyzed the composition of low-density lipoprotein (LDL) and HDL subpopulations in such individuals. The LipoPrint(©) system (Quantimetrix, USA) based on non-denaturing, linear polyacrylamide gel electrophoresis was used to separate and measure LDL and HDL subclasses in fresh-frozen serum samples from patients with mutations of glucokinase or …

AdultMalemedicine.medical_specialtyAdolescentEndocrinology Diabetes and MetabolismBiologyLipid subpopulationsYoung Adultchemistry.chemical_compoundEndocrinologyMonogenic diabetesInternal medicineDiabetes mellitusGlucokinasemedicineInternal MedicineHumansHepatocyte Nuclear Factor 1-alphaChildType 1 diabetesmedicine.diagnostic_testCholesterolGlucokinaseCholesterol HDLCase-control studynutritional and metabolic diseasesCholesterol LDLGeneral Medicinemedicine.diseaseLipoproteins LDLDiabetes Mellitus Type 1EndocrinologychemistryCase-Control StudiesMetabolic control analysisMODYOriginal ArticleFemalelipids (amino acids peptides and proteins)Lipoproteins HDLLipid profileLipoproteinActa Diabetologica
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Hepatic amino acid uptake is decreased in lactating rats. In vivo and in vitro studies.

1994

To study the redistribution of amino acids to the mammary gland during lactation we used lactating and virgin rats fed liquid diets. Virgin rats were divided in two groups: one group was fed daily a diet containing the same amount of protein that was consumed the previous day by lactating rats (high protein diet-fed rats), and the other virgin group was fed the normal liquid diet (control). The hepatic availability of amino acids was significantly higher in the lactating rats than in the other two groups, but the uptake and fractional extraction of amino acids by the liver were lower in lactating rats than in the high protein-fed virgin controls. When primary hepatocyte cultures were used, …

medicine.medical_specialtyanimal structuresLiquid dietMedicine (miscellaneous)Biological AvailabilityHigh-protein dietBiologymedicine.disease_causeLactationInternal medicinemedicineAnimalsLactationTissue DistributionAmino AcidsRats WistarIncubationCells Culturedchemistry.chemical_classificationNutrition and DieteticsMetabolismProlactinAmino acidProlactinRatsmedicine.anatomical_structureEndocrinologychemistryLiverHepatocyteFemaleDietary ProteinsLiver CirculationThe Journal of nutrition
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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Model Based Targeting of IL-6-Induced Inflammatory Responses in Cultured Primary Hepatocytes to Improve Application of the JAK Inhibitor Ruxolitinib

2017

IL-6 is a central mediator of the immediate induction of hepatic acute phase proteins (APP) in the liver during infection and after injury, but increased IL-6 activity has been associated with multiple pathological conditions. In hepatocytes, IL-6 activates JAK1-STAT3 signaling that induces the negative feedback regulator SOCS3 and expression of APPs. While different inhibitors of IL-6-induced JAK1-STAT3-signaling have been developed, understanding their precise impact on signaling dynamics requires a systems biology approach. Here we present a mathematical model of IL-6-induced JAK1-STAT3 signaling that quantitatively links physiological IL-6 concentrations to the dynamics of IL-6-induced …

0301 basic medicineRuxolitinibruxolitinibPhysiologySystems biologyRegulatorBiologyPharmacology: Biochemistry biophysics & molecular biology [F05] [Life sciences]lcsh:Physiology03 medical and health sciencesMediatoracute phase responsePhysiology (medical)medicineSOCS3primary hepatocytes: Biochimie biophysique & biologie moléculaire [F05] [Sciences du vivant]Original ResearchIL-6lcsh:QP1-981Acute-phase proteinmathematical modelingJAK-STAT signaling pathwayCell biology030104 developmental biologySignal transductionmedicine.drugFrontiers in Physiology
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Effects of a high-fat diet on energy metabolism and ROS production in rat liver.

2011

International audience; BACKGROUND & AIMS: A high-fat diet affects liver metabolism, leading to steatosis, a complex disorder related to insulin resistance and mitochondrial alterations. Steatosis is still poorly understood since diverse effects have been reported, depending on the different experimental models used. METHODS: We hereby report the effects of an 8 week high-fat diet on liver energy metabolism in a rat model, investigated in both isolated mitochondria and hepatocytes. RESULTS: Liver mass was unchanged but lipid content and composition were markedly affected. State-3 mitochondrial oxidative phosphorylation was inhibited, contrasting with unaffected cytochrome content. Oxidative…

Mitochondrial ROSMaleTranscription GeneticMESH : Reactive Oxygen SpeciesMitochondria LiverMESH : HepatocytesMitochondrionOxidative PhosphorylationMESH: Hepatocytes0302 clinical medicineMESH: Membrane Potential MitochondrialCitrate synthaseMESH: AnimalsBeta oxidationMESH : Electron Transport2. Zero hungerMembrane Potential Mitochondrial0303 health sciencesMESH : RatsAdenine nucleotide translocatorMESH: Energy MetabolismMESH: Reactive Oxygen SpeciesLipidsBiochemistryLiverMESH: Dietary FatsMitochondrial matrix030220 oncology & carcinogenesisBody CompositionMESH : Oxidative PhosphorylationATP–ADP translocaseMESH: Mitochondria LiverMESH: RatsMESH : Body CompositionMESH : MaleOxidative phosphorylationBiologyMESH : Rats WistarElectron Transport03 medical and health sciencesMESH: Oxidative Phosphorylation[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats WistarMESH: Electron Transport[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyHepatologyMESH: Transcription GeneticMESH : Transcription GeneticMESH : LiverMESH : LipidsMESH: Body CompositionMESH: Rats WistarMESH: LipidsDietary FatsMESH: MaleRatsMESH : Energy MetabolismMESH : Membrane Potential MitochondrialMESH : Mitochondria Liverbiology.proteinHepatocytesMESH : AnimalsEnergy MetabolismReactive Oxygen SpeciesMESH : Dietary FatsMESH: Liver
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Hepatocyte cell lines: their use, scope and limitations in drug metabolism studies.

2006

Gaining knowledge on the metabolism of a drug, the enzymes involved and its inhibition or induction potential is a necessary step in pharmaceutical development of new compounds. Primary human hepatocytes are considered a cellular model of reference, as they express the majority of drug-metabolising enzymes, respond to enzyme inducers and are capable of generating in vitro a metabolic profile similar to what is found in vivo. However, hepatocytes show phenotypic instability and have a restricted accessibility. Different alternatives have been explored in the past recent years to overcome the limitations of primary hepatocytes. These include immortalisation of adult or fetal human hepatic cel…

PharmacologyCell fusionCell Culture TechniquesDrug Evaluation PreclinicalReproducibility of ResultsGeneral MedicineBiologyToxicologyCell biologyCell LineXenobioticsmedicine.anatomical_structureBiochemistryDownregulation and upregulationCell cultureHepatocytemedicineHepatic stellate cellHepatocytesAnimalsHumansProgenitor cellCellular modelDrug metabolismCell Line TransformedExpert opinion on drug metabolismtoxicology
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Melatonin induces transcriptional regulation of Bim by FoxO3a in HepG2 cells

2012

Background: Melatonin induces apoptosis in many different cancer cell lines, including hepatocellular carcinoma cells. However, the responsible pathways have not been clearly elucidated. A member of the forkhead transcription factors' family, FoxO3a, has been implicated in the expression of the proapoptotic protein Bim (a Bcl-2-interacting mediator of cell death). In this study, we used human HepG2 liver cancer cells as an in vitro model to investigate whether melatonin treatment induces Bim through regulation by the transcription factor FoxO3a. Methods: Cytotoxicity of melatonin was compared in HepG2 hepatoblastoma cells and primary human hepatocytes. Proapoptotic Bim expression was analys…

Transcriptional ActivationCancer Researchmedicine.medical_specialtyProgrammed cell deathSmall interfering RNACarcinoma HepatocellularTranscription GeneticApoptosisFoxO3amelatoninBiologyGenetics & GenomicsMelatoninDownregulation and upregulationCell Line TumorProto-Oncogene ProteinsInternal medicinemedicineTranscriptional regulationHumansGene silencingBimPhosphorylationRNA Small InterferingPromoter Regions GeneticTranscription factorBinding SitesBcl-2-Like Protein 11Forkhead Box Protein O3Membrane ProteinsForkhead Transcription FactorsHep G2 Cellshepatocellular carcinomaCell biologyEndocrinologyOncologyHepatocytesRNA Interferencebiological phenomena cell phenomena and immunityApoptosis Regulatory ProteinsChromatin immunoprecipitationProtein Bindingmedicine.drugBritish Journal of Cancer
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Bis(hydroxyphenyl)methane-bisphenol F-metabolism by the HepG2 human hepatoma cell line and cryopreserved human hepatocytes

2011

author cannot archive publisher's version/PDF; International audience; Bisphenol F (BPF) is present in the environment and as a contaminant of food. Humans may, therefore, be exposed to BPF, and an assessment of this risk is required. BPF has been shown to have genotoxic and endocrine-disruptor properties in a human hepatoma cell line (HepG2), which is a model system for studies of xenobiotic toxicity. In this study, we investigated the ability of HepG2 cells to biotransform BPF, because metabolism may affect the observed effects of BPF, and we compared this metabolic capacity with that of human hepatocytes. Cells were incubated for 24 hours with [(3)H]-BPF. The culture medium was then conc…

Bisphenol FHealth Toxicology and MutagenesisestrogenicityCell Culture Techniques010501 environmental sciencesToxicology01 natural sciencesMass SpectrometryCryopreservationchemistry.chemical_compoundenzyme level[SDV.IDA]Life Sciences [q-bio]/Food engineeringperformance liquid chromatographyratLuciferasesinductionChromatography High Pressure Liquidendocrine disruptor0303 health sciencesfood and environmental contaminantMolecular StructureHep G2 CellsGeneral MedicineBiochemistryHepg2 cellsin vitro modeldispositionToxicityEnvironmental Pollutantsliver enzymebiotransformationGlucuronidePlasmidsBiologyTransfectionliver03 medical and health sciencesHumans[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process EngineeringBenzhydryl Compounds030304 developmental biology0105 earth and related environmental sciencesCryopreservationPharmacologyChemical Health and Safetyactivitybisphenol aEstrogen Receptor alphaPublic Health Environmental and Occupational HealthMetabolismbeta-GalactosidaseHepatoma cell linechemistryHepatocytesXenobiotic
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