Search results for "hepatocyte"

showing 10 items of 369 documents

Hnf4α is a key gene that can generate columnar metaplasia in oesophageal epithelium

2017

AbstractBarrett's metaplasia is the only known morphological precursor to oesophageal adenocarcinoma and is characterized by replacement of stratified squamous epithelium by columnar epithelium. The cell of origin is uncertain and the molecular mechanisms responsible for the change in cellular phenotype are poorly understood. We therefore explored the role of two transcription factors, Cdx2 and HNF4α in the conversion using primary organ cultures. Biopsy samples from cases of human Barrett's metaplasia were analysed for the presence of CDX2 and HNF4α. A new organ culture system for adult murine oesophagus is described. Using this, Cdx2 and HNF4α were ectopically expressed by adenoviral infe…

0301 basic medicineMalePathologyCancer ResearchEsophageal NeoplasmsBiopsyEpitheliumMice0302 clinical medicineMetaplasiaCDX2 Transcription FactorCDX2CàncerOesophageal cancerAnatomyNeoplasm ProteinsBarrett's oesophagusGene Expression Regulation Neoplasticmedicine.anatomical_structureHepatocyte Nuclear Factor 4Loricrin/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_being030211 gastroenterology & hepatologymedicine.symptomVillinHepatocyte nuclear factor 4-alphaAdultmedicine.medical_specialtyStratified squamous epitheliumBiologyAdenocarcinomaOrgan cultureArticle03 medical and health sciencesBarrett EsophagusEsophagusOrgan Culture TechniquesSDG 3 - Good Health and Well-beingmedicineAnimalsHumansMolecular BiologyHNF4αMetaplasiaHistologiaCell BiologyEpitheliumdigestive system diseases030104 developmental biologybiology.proteinEctopic expressionDevelopmental Biology
researchProduct

Mitochondrial Fatty Acid β-Oxidation Inhibition Promotes Glucose Utilization and Protein Deposition through Energy Homeostasis Remodeling in Fish.

2020

BACKGROUND: Fish cannot use carbohydrate efficiently and instead utilize protein for energy supply, thus limiting dietary protein storage. Protein deposition is dependent on protein turnover balance, which correlates tightly with cellular energy homeostasis. Mitochondrial fatty acid β-oxidation (FAO) plays a crucial role in energy metabolism. However, the effect of remodeled energy homeostasis caused by inhibited mitochondrial FAO on protein deposition in fish has not been intensively studied. OBJECTIVES: This study aimed to identify the regulatory role of mitochondrial FAO in energy homeostasis maintenance and protein deposition by studying lipid, glucose, and protein metabolism in fish. M…

0301 basic medicineMaleProtein metabolismMedicine (miscellaneous)MitochondrionEnergy homeostasis03 medical and health scienceschemistry.chemical_compoundNile tilapia0302 clinical medicineAdjuvants ImmunologicmedicineAnimalsHomeostasisInsulinCarnitineProtein kinase ACells CulturedZebrafishNutrition and DieteticsbiologyCarnitine O-PalmitoyltransferaseChemistryFatty AcidsProtein turnoverProteinsMetabolismCichlidsDNACytochromes bbiology.organism_classificationMitochondria030104 developmental biologyGlucoseBiochemistryMutationHepatocytesNutrient Physiology Metabolism and Nutrient-Nutrient InteractionsEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgerymedicine.drugMethylhydrazinesThe Journal of nutrition
researchProduct

Inter-individual differences in the susceptibility of primary human hepatocytes towards drug-induced cholestasis are compound and time dependent.

2018

Abstract Cholestasis represents a major subtype of drug-induced liver injury and novel preclinical models for its prediction are needed. Here we used primary human hepatocytes (PHH) from different donors in 2D-sandwich (2D-sw) and/or 3D-spheroid cultures to study inter-individual differences in the response towards cholestatic hepatotoxins after short-term (48–72 hours) and long-term repeated exposures (14 days). The cholestatic liabilities of drugs were determined by comparing cell viability upon exposure to the highest non-cytotoxic drug concentration in the presence and absence of a non-cytotoxic concentrated bile acid mixture. In 2D-sw culture, cyclosporine A and amiodarone presented cl…

0301 basic medicineMaleTime Factorsmedicine.drug_classPrimary Cell CulturePharmacologyToxicologyRisk Assessment03 medical and health sciencesCholestasisSpheroids CellularmedicineHumansChlorpromazineCells CulturedAgedLiver injuryCholestasisBile acidDose-Response Relationship Drugbusiness.industryBile CanaliculiHepatotoxinTroglitazoneGeneral MedicineMiddle Agedmedicine.diseaseBosentan3. Good health030104 developmental biologyBiological Variation PopulationToxicityHepatocytesFemaleChemical and Drug Induced Liver Injurybusinessmedicine.drugToxicology letters
researchProduct

Simultaneous Inhibition of Peripheral CB1R and iNOS Mitigates Obesity-Related Dyslipidemia Through Distinct Mechanisms.

2020

Diabetic dyslipidemia, characterized by increased plasma triglycerides and decreased HDL cholesterol levels, is a major factor contributing to nonalcoholic steatohepatitis and cardiovascular risk in type 2 diabetes. Activation of the cannabinoid-1 receptor (CB1R) and activation of inducible nitric oxide synthase (iNOS) are associated with nonalcoholic steatohepatitis progression. Here, we tested whether dual-targeting inhibition of hepatic CB1R and iNOS improves diabetic dyslipidemia in mice with diet-induced obesity (DIO mice). DIO mice were treated for 14 days with (S)-MRI-1867, a peripherally restricted hybrid inhibitor of CB1R and iNOS. (R)-MRI-1867, the CB1R-inactive stereoisomer that …

0301 basic medicineMaleVery low-density lipoproteinEndocrinology Diabetes and MetabolismNitric Oxide Synthase Type II[SDV.BC.IC] Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB][SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMice0302 clinical medicineReceptor Cannabinoid CB1[SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB]Receptor[SDV.BBM.BC] Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Cells Cultured[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismbiology[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]Nitric oxide synthaseLiver[SDV.SP.PHARMA] Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologyKexinlipids (amino acids peptides and proteins)medicine.medical_specialty[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]LipoproteinsImmunoblotting030209 endocrinology & metabolismReal-Time Polymerase Chain Reaction03 medical and health sciencesInternal medicineCommentariesInternal MedicinemedicineAnimalsObesity[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biochemistry [q-bio.BM]Dyslipidemiasbusiness.industry[SDV.OT] Life Sciences [q-bio]/Other [q-bio.OT]PCSK9nutritional and metabolic diseases[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and Gastroenterology[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologymedicine.diseaseLipid Metabolism[SDV.MHEP.HEG] Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseLDL receptorbiology.proteinHepatocytes[SDV.SP.PHARMA]Life Sciences [q-bio]/Pharmaceutical sciences/PharmacologySteatosisbusinessDyslipidemia
researchProduct

Recombinant human hepatocyte growth factor provides protective effects in cerulein-induced acute pancreatitis in mice.

2018

Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c-Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein-induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip…

0301 basic medicineMalemedicine.medical_specialtyNecrosisPhysiologyClinical BiochemistryInflammationApoptosismedicine.disease_causeProtective AgentsAntioxidantsProinflammatory cytokine03 medical and health sciencesMiceInternal medicineEdemamedicineAnimalsHumansbusiness.industryHepatocyte Growth FactorCell BiologyProto-Oncogene Proteins c-metmedicine.diseaseGlutathioneSurvival AnalysisRecombinant ProteinsDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyPancreatitisAcute pancreatitisPancreatitisHepatocyte growth factormedicine.symptombusinessOxidative stressCeruletidemedicine.drugSignal TransductionJournal of cellular physiology
researchProduct

Bioactive triterpenes of protium heptaphyllum gum resin extract display cholesterol-lowering potential

2021

Hypercholesterolemia is one of the major causes of cardiovascular disease, the risk of which is further increased if other forms of dyslipidemia occur. Current therapeutic strategies include changes in lifestyle coupled with drug administration. Statins represent the most common therapeutic approach, but they may be insufficient due to the onset of resistance mechanisms and side effects. Consequently, patients with mild hypercholesterolemia prefer the use of food supplements since these are perceived to be safer. Here, we investigate the phytochemical profile and cholesterol-lowering potential of Protium heptaphyllum gum resin extract (PHE). Chemical characterization via HPLC-APCI-HRMS2 and…

0301 basic medicineModels MolecularProtein ConformationDrug Evaluation Preclinical030204 cardiovascular system & hematologyPharmacologyPPARαTerpenelcsh:ChemistryPCSK9chemistry.chemical_compound0302 clinical medicineCatalytic DomainSettore BIO/10 - BiochimicaPlant Gumslcsh:QH301-705.5SpectroscopyChromatography High Pressure LiquidFlame IonizationMonacolinChemistryAnticholesteremic AgentsGeneral MedicineComputer Science ApplicationsMolecular Docking SimulationCholesterolPhytochemicalMolecular dockinglipids (amino acids peptides and proteins)Breu brancoStatinmedicine.drug_classHypercholesterolemiaArticleCatalysisGas Chromatography-Mass SpectrometryInorganic Chemistry03 medical and health sciencesNutraceuticalmedicineHumansLovastatinPhysical and Theoretical ChemistryMolecular BiologyOleananeHMGCREnzymatic activityCholesterolPCSK9Organic ChemistryStatinSettore CHIM/08 - Chimica FarmaceuticaTriterpenes030104 developmental biologyhypercholesterolemia; gene expression; HMGCR; PCSK9; PPARα; enzymatic activity; molecular docking; statin; monacolin; breu brancolcsh:Biology (General)lcsh:QD1-999Breu branco; Enzymatic activity; Gene expression; HMGCR; Hypercholesterolemia; Molecular docking; Monacolin; PCSK9; PPARα; StatinLDL receptorDietary SupplementsHepatocytesSettore BIO/14 - FarmacologiaGene expressionHydroxymethylglutaryl-CoA Reductase InhibitorsResins PlantHydrogen
researchProduct

Levosimendan protects human hepatocytes from ischemia-reperfusion injury.

2017

Background Ischemia-reperfusion injury (IRI) is a major challenge in liver transplantation. The mitochondrial pathway plays a pivotal role in hepatic IRI. Levosimendan, a calcium channel sensitizer, was shown to attenuate apoptosis after IRI in animal livers. The aim of this study was to investigate the effect of levosimendan on apoptosis in human hepatocytes. Methods Primary human hepatocytes were either exposed to hypoxia or cultured under normoxic conditions. After the hypoxic phase, reoxygenation was implemented and cells were treated with different concentrations of levosimendan (10ng/ml, 100ng/ml, 1000ng/ml). The overall metabolic activity of the cells was measured using 3-(4,5-dimeth…

0301 basic medicineNecrosisCritical Care and Emergency Medicinelcsh:MedicineApoptosis030204 cardiovascular system & hematologyBiochemistry0302 clinical medicineAnimal CellsMedicine and Health SciencesEnzyme assaysColorimetric assayslcsh:ScienceBioassays and physiological analysisCells CulturedEnergy-Producing Organellesbcl-2-Associated X ProteinMultidisciplinaryMTT assaybiologyCell DeathMitochondriaPyridazinesLiverCell ProcessesReperfusion Injurymedicine.symptomCellular TypesAnatomyCellular Structures and Organellesmedicine.drugResearch Articlemedicine.medical_specialtyCell PhysiologyIschemiaCardiologySurgical and Invasive Medical ProceduresBioenergetics03 medical and health sciencesDigestive System ProceduresBcl-2-associated X proteinInternal medicinemedicineHumansMTT assayddc:610SimendanHeart FailureTransplantationbusiness.industrylcsh:RHydrazonesBiology and Life SciencesLevosimendanCell BiologyOrgan TransplantationHypoxia (medical)medicine.diseaseLiver TransplantationCell MetabolismResearch and analysis methods030104 developmental biologyEndocrinologyApoptosisReperfusionBiochemical analysisbiology.proteinHepatocyteslcsh:QbusinessReperfusion injuryPloS one
researchProduct

Increased liver carcinogenesis and enrichment of stem cell properties in livers of Dickkopf 2 (Dkk2) deleted mice.

2013

// Thorsten Maass 1 , Jens Marquardt 2 , Ju-Seog Lee 3 , Markus Krupp 4 , Peter Scholz-Kreisel 2 , Carolin Mogler 5 , Peter Schirmacher 5 , Martina Muller 1 , Heiner Westphal 6 , Peter R. Galle 2 , Andreas Teufel 1 1 Department of Internal Medicine I, University of Regensburg, Regensburg, Germany 2 I. Department of Medicine, University Medical Center Mainz, Mainz, Germany 3 Cancer Biology Program, MD Anderson Cancer Center, Houston, TX, USA 4 Department of Informatics, Johannes Gutenberg University Mainz, Mainz, Germany 5 Institute of Pathology, University of Heidelberg, Heidelberg, Germany 6 Laboratory of Mammalian Genes and Development, National Institute of Child Health and Human Develop…

0301 basic medicinePathologymedicine.medical_specialtyCarcinogenesisBiologymedicine.disease_causeTranscriptome03 medical and health sciencesMicestem cellsmedicineAtypiaAnimalsHumansGene Regulatory Networksprognostic signatureGeneWnt Signaling PathwayMice Knockouttranscriptomics profilingLiver CarcinogenesisDkk2Liver NeoplasmsGastroenterologyWnt signaling pathwaymedicine.diseaseMolecular biologyMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureOncologyHepatocyteCancer researchNeoplastic Stem CellsIntercellular Signaling Peptides and ProteinsStem cellLiver cancerCarcinogenesisgenetic signatureResearch PaperOncotarget
researchProduct

Apoptosis of Hepatocytes: Relevance for HIV-Infected Patients under Treatment.

2021

Due to medical advances over the past few decades, human immunodeficiency virus (HIV) infection, once a devastatingly mortal pandemic, has become a manageable chronic condition. However, available antiretroviral treatments (cART) cannot fully restore immune health and, consequently, a number of inflammation-associated and/or immunodeficiency complications have manifested themselves in treated HIV-infected patients. Among these chronic, non-AIDS (acquired immune deficiency syndrome)-related conditions, liver disease is one of the deadliest, proving to be fatal for 15–17% of these individuals. Aside from the presence of liver-related comorbidities, including metabolic disturbances and co-infe…

0301 basic medicineProgrammed cell deathChronic conditionantiretroviral drugs; apoptosis; hepatic cell death; HIV; liver; toxicityInflammationApoptosisHIV InfectionsReviewliverModels Biological03 medical and health sciencesLiver disease0302 clinical medicineImmune systemAntiretroviral Therapy Highly ActivemedicineHumans030212 general & internal medicinelcsh:QH301-705.5antiretroviral drugsImmunodeficiencybusiness.industryapoptosisHIVtoxicityGeneral Medicinemedicine.diseasehepatic cell death030104 developmental biologylcsh:Biology (General)LiverApoptosisImmunologyUnfolded protein responseHepatocytesmedicine.symptombusinessCells
researchProduct

Kinase-independent functions of RIPK1 regulate hepatocyte survival and liver carcinogenesis.

2017

The mechanisms that regulate cell death and inflammation play an important role in liver disease and cancer. Receptor-interacting protein kinase 1 (RIPK1) induces apoptosis and necroptosis via kinase-dependent mechanisms and exhibits kinase-independent prosurvival and proinflammatory functions. Here, we have used genetic mouse models to study the role of RIPK1 in liver homeostasis, injury, and cancer. While ablating either RIPK1 or RelA in liver parenchymal cells (LPCs) did not cause spontaneous liver pathology, mice with combined deficiency of RIPK1 and RelA in LPCs showed increased hepatocyte apoptosis and developed spontaneous chronic liver disease and cancer that were independent of TNF…

0301 basic medicineProgrammed cell deathLiver tumorCell SurvivalNecroptosisMice TransgenicBiologyChronic liver diseaseProinflammatory cytokine03 medical and health sciencesLiver diseaseMiceLiver Neoplasms ExperimentalmedicineAnimalsDiethylnitrosamineKinase activityTranscription Factor RelAGeneral Medicinemedicine.disease3. Good healthNeoplasm Proteins030104 developmental biologymedicine.anatomical_structureCell Transformation NeoplasticReceptors Tumor Necrosis Factor Type IHepatocyteReceptor-Interacting Protein Serine-Threonine KinasesCancer researchHepatocytesSignal TransductionResearch ArticleThe Journal of clinical investigation
researchProduct