Search results for "hepatocyte"

showing 10 items of 369 documents

Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors

2014

Apoptosis signaling is involved in both physiological tissue homeostasis and acute and chronic diseases. The role of regulatory apoptosis signaling molecules and their organ-specific functions are less defined. Therefore, we investigated the loss of the anti-apoptotic cellular FLICE-inhibitory protein (cFLIP) and the mechanisms of the resulting lethal organ failure in vivo using inducible knockout mice. These were generated by crossing floxed cFLIP mice to a tamoxifen inducible Rosa26-creERT2 mouse strain. Death following global loss of cFLIP resulted from liver failure, accumulation of M1-polarized macrophages and accompanying hepatic cell death and inflammation. Apoptosis was also promine…

Programmed cell deathCASP8 and FADD-Like Apoptosis Regulating ProteinMice TransgenicInflammationBiologyMiceImmune systemmedicineAnimalsMolecular BiologyTissue homeostasisOriginal PaperInnate immune systemMacrophagesMembrane ProteinsCell BiologyLiver Failure AcuteImmunity InnateCell biologyToll-Like Receptor 4TransplantationApoptosisToll-Like Receptor 9Stimulator of interferon genesHepatocytesmedicine.symptomCell Death & Differentiation
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Knockout of myeloid cell leukemia-1 induces liver damage and increases apoptosis susceptibility of murine hepatocytes

2008

Apoptosis, or programmed cell death, regulates tissue development and homeostasis in multi-cellular organisms. Extrinsic or intrinsic death signals activate pro-apoptotic pathways, resulting in the activation of caspases and finally in cell death. An important event during apoptosis process is the permeabilization of the outer mitochondrial membrane (OMM). Integrity of the OMM is regulated by the Bcl-2 protein family, which is divided into three groups: anti-apoptotic members Bcl-2, Bcl-xL and myeloid cell leukemia-1 (Mcl-1), pro-apoptotic multidomain members Bax and Bak, and pro-apoptotic BH3-only proteins. Mitochondrial activation is regulated by selective interactions of Bcl-2 proteins v…

Programmed cell deathGenotypeCellular differentiation610 Medicine & healthApoptosisBiologyPolymerase Chain ReactionArticleMiceimmune system diseases10049 Institute of Pathology and Molecular Pathologyhemic and lymphatic diseasesmedicineAnimalsAspartate AminotransferasesneoplasmsDNA PrimersHepatologyCaspase 3Alanine TransaminaseCell DifferentiationDNAFas receptorCell biologyMyeloid Cell Leukemia Sequence 1 ProteinHaematopoiesisGene Expression RegulationLiverProto-Oncogene Proteins c-bcl-2ApoptosisHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinRNA2721 HepatologyHepatocyte growth factorStem cellmedicine.drugHepatology
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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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In vivo real-time imaging of the liver with confocal endomicroscopy permits visualization of the temporospatial patterns of hepatocyte apoptosis.

2011

Apoptosis is a dynamic process of programmed cell death and is involved in multiple diseases. However, its mechanisms and sequence of events are still incompletely understood, partly because of the inability to visualize single cells continuously in vivo. The aim of the present study was to monitor hepatocyte apoptosis with confocal endomicroscopy in living rodents. In 73 anaesthetized mice, apoptotic liver injury was induced by injection of the CD95-agonistic antibody Jo2. Individual hepatocytes were followed for up to 240 min with a handheld confocal probe (FIVE1; Optiscan) providing 0.7 μm resolution (1,000-fold magnification). Different fluorescence staining protocols were used for cell…

Programmed cell deathMicroscopy ConfocalHepatologyPhysiologyConfocalGastroenterologyReal time imagingApoptosisEndoscopyBiologyCell biologylaw.inventionMiceLiverIn vivoApoptosisConfocal microscopylawPhysiology (medical)EndomicroscopyHepatocytesAnimalsHepatocyte apoptosisAmerican journal of physiology. Gastrointestinal and liver physiology
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Differential Roles of JNK in ConA/GalN and ConA-Induced Liver Injury in Mice

2008

Tumor necrosis factor-alpha-mediated liver injury can be induced by several different means; however, the signaling events and mechanisms of cell death are likely different. We investigated the mechanism of both apoptotic and necrotic hepatocyte cell death as well as the role of c-Jun NH2-terminal kinase (JNK) in the ConA and ConA/D-galactosamine (GalN) models of murine liver injury. ConA alone induced primarily necrotic cell death with no caspase activation, whereas ConA/GalN induced apoptosis in addition to necrotic cell death. The bi-modal death pattern in the ConA/GalN model was confirmed by the use of transgenic mice expressing a dominant-negative form of Fas-associated death domain in…

Programmed cell deathNecrosisFas-Associated Death Domain ProteinApoptosisGalactosamineMitochondria Liverchemical and pharmacologic phenomenaCaspase 8Pathology and Forensic MedicineMiceNecrosisConcanavalin AmedicineAnimalsPhosphorylationDeath domainLiver injuryCaspase 8biologyLiver DiseasesJNK Mitogen-Activated Protein Kinasesmedicine.diseaseMolecular biologyEnzyme ActivationMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureConcanavalin AApoptosisHepatocytebiology.proteinMutant ProteinsChemical and Drug Induced Liver Injurymedicine.symptomGene DeletionRegular ArticlesBH3 Interacting Domain Death Agonist ProteinThe American Journal of Pathology
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Hepatocyte-specific deletion of the antiapoptotic protein myeloid cell leukemia-1 triggers proliferation and hepatocarcinogenesis in mice

2010

Regulation of hepatocellular apoptosis is crucial for liver homeostasis. Increased sensitivity of hepatocytes toward apoptosis results in chronic liver injury, whereas apoptosis resistance is linked to hepatocarcinogenesis and nonresponsiveness to therapy-induced cell death. Recently, we have demonstrated an essential role of the antiapoptotic Bcl-2 family member Myeloid cell leukemia-1 (Mcl-1) in hepatocyte survival. In mice lacking Mcl-1 specifically in hepatocytes (Mcl-1Δhep), spontaneous apoptosis caused severe liver damage. Here, we demonstrate that chronically increased apoptosis of hepatocytes coincides with strong hepatocyte proliferation resulting in hepatocellular carcinoma (HCC).…

Programmed cell deathPathologymedicine.medical_specialty10208 Institute of NeuropathologyApoptosis610 Medicine & health10071 Functional Genomics Center ZurichBiologyArticleMiceLiver Neoplasms Experimental10049 Institute of Pathology and Molecular PathologySurvivinmedicineAnimalsneoplasmsCell ProliferationChromosome AberrationsMice KnockoutHepatologyCell growthLiver cellmedicine.diseaseMyeloid Cell Leukemia Sequence 1 ProteinLeukemiamedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisHepatocyteHepatocytesCancer researchMyeloid Cell Leukemia Sequence 1 Protein570 Life sciences; biology2721 HepatologyU7 Systems Biology / Functional GenomicsHepatology
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Circulating haemopoietic and endothelial progenitor cells are decreased in COPD

2006

Circulating CD34+ cells are haemopoietic progenitors that may play a role in tissue repair. No data are available on circulating progenitors in chronic obstructive pulmonary disease (COPD). Circulating CD34+ cells were studied in 18 patients with moderate-to-severe COPD (age: mean+/-sd 68+/-8 yrs; forced expiratory volume in one second: 48+/-12% predicted) and 12 controls, at rest and after endurance exercise. Plasma concentrations of haematopoietic growth factors (FMS-like tyrosine kinase 3 (Flt3) ligand, kit ligand), markers of hypoxia (vascular endothelial growth factor (VEGF)) and stimulators of angiogenesis (VEGF, hepatocyte growth factor (HGF)) and markers of systemic inflammation (tu…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyAngiogenesisCD34Antigens CD34cd34Settore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - Fisiologiachronic obstructive pulmonary diseaseimmunologyPulmonary Disease Chronic Obstructivecd34+ cellscd34+cellschemistry.chemical_compoundantigensbloodstem cellsInternal medicinegrowth factorsmiddle agedMedicineProgenitor cellhumansCD34+ cells chronic obstructive pulmonary disease exercise growth factors hypoxiacell countpulmonary diseaseCOPDchronic obstructiveexercisehypoxiabusiness.industryaged; antigens; blood; cd34; cd34+ cells; cd34+cells; cell count; chronic obstructive; chronic obstructive pulmonary disease; endothelial cells; exercise; growth factors; hematopoietic stem cells; humans; hypoxia; immunology; middle aged; pulmonary disease; stem cellsHypoxia (medical)medicine.diseaseendothelial cellshematopoietic stem cellsEndothelial stem cellVascular endothelial growth factoragedEndocrinologychemistryHepatocyte growth factormedicine.symptombusinessmedicine.drugEuropean Respiratory Journal
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Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice.

2001

Mutations that influence the repair of oxidative DNA modifications are expected to increase the steady-state (background) levels of these modifications and thus create a mutator phenotype that predisposes to malignant transformation. We have analysed the steady-state levels and repair kinetics of oxidative DNA modifications in cells of homozygous ogg1(-/-) null mice, which are deficient in Ogg1 protein, a DNA repair glycosylase that removes the miscoding base 8-hydroxyguanine (8-oxoG) from the genome. Oxidative purine modifications including 8-oxoG were quantified by means of an alkaline elution assay in combination with Fpg protein, the bacterial functional analogue of Ogg1 protein. In pri…

PurineMaleCancer ResearchGuanineDNA RepairOxidative phosphorylationBiologymedicine.disease_causeMalignant transformationchemistry.chemical_compoundMiceTranscription (biology)medicineAnimalsN-Glycosyl HydrolasesMice KnockoutCell growthAge FactorsGeneral MedicineDNAFibroblastsMolecular biologyOxygenOxidative StresschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseOrgan SpecificityImmunologyHepatocytesOxidative stressDNACell DivisionDNA DamageCarcinogenesis
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Factors that influence the quality of metabolomics data in in vitro cell toxicity studies: a systematic survey

2021

Abstract REACH (Registration, Evaluation, Authorization and Restriction of Chemicals) is a global strategy and regulation policy of the EU that aims to improve the protection of human health and the environment through the better and earlier identification of the intrinsic properties of chemical substances. It entered into force on 1st June 2007 (EC 1907/2006). REACH and EU policies plead for the use of robust high-throughput "omic" techniques for the in vitro investigation of the toxicity of chemicals that can provide an estimation of their hazards as well as information regarding the underlying mechanisms of toxicity. In agreement with the 3R’s principles, cultured cells are nowadays wide…

Quality ControlHEPATOTOXICITYSciencemedia_common.quotation_subjectDiseasesComputational biologyMETABOLISMBiologyHEPATOCYTESCitric AcidArticleXenobioticsProductes químicschemistry.chemical_compoundMetabolomicsMedical researchCell Line TumorMetabolomeHumansMetabolomicsSPECTROMETRY DATAQuality (business)HEPARG CELLSAcetaminophenmedia_commonBATCH EFFECT CORRECTIONMultidisciplinaryFATTY-ACIDDrug discoveryValproic AcidQRReproducibility of ResultsHep G2 CellsIn vitroBioactive compoundGLUTAMINEMetabolic pathwayLiverchemistryToxicityMetabolomeMedicineCURRENT STATEChemical and Drug Induced Liver InjuryXenobioticMetabolic Networks and PathwaysBiomarkersVALPROATEScientific Reports
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New active drugs against liver stages of Plasmodium predicted by molecular topology.

2008

ABSTRACT We conducted a quantitative structure-activity relationship (QSAR) study based on a database of 127 compounds previously tested against the liver stage of Plasmodium yoelii in order to develop a model capable of predicting the in vitro antimalarial activities of new compounds. Topological indices were used as structural descriptors, and their relation to antimalarial activity was determined by using linear discriminant analysis. A topological model consisting of two discriminant functions was created. The first function discriminated between active and inactive compounds, and the second identified the most active among the active compounds. The model was then applied sequentially t…

Quantitative structure–activity relationshipStereochemistryAntiparasiticmedicine.drug_classModels BiologicalAuto-immunity transplantation and immunotherapy [N4i 4]AntimalarialsMiceStructure-Activity RelationshipParasitic Sensitivity Testsparasitic diseasesmedicineAnimalsHumansStructure–activity relationshipPharmacology (medical)PharmacologybiologyPoverty-related infectious diseases [N4i 3]Plasmodium falciparumPlasmodium yoeliibiology.organism_classificationIn vitroInfectious Diseasesmedicine.anatomical_structureLiverBiochemistrySusceptibilityHepatocyteHepatocytesMicrobial pathogenesis and host defense [UMCN 4.1]Infection and autoimmunity [NCMLS 1]Plasmodium yoeliiFunction (biology)Immunity infection and tissue repair [NCMLS 1]
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