Search results for "Stellate cell"

showing 10 items of 106 documents

Spike-in SILAC proteomic approach reveals the vitronectin as an early molecular signature of liver fibrosis in hepatitis C infections with hepatic ir…

2014

Hepatitis C virus (HCV)-induced iron overload has been shown to promote liver fibrosis, steatosis, and hepatocellular carcinoma. The zonal-restricted histological distribution of pathological iron deposits has hampered the attempt to perform large-scale in vivo molecular investigations on the comorbidity between iron and HCV. Diagnostic and prognostic markers are not yet available to assess iron overload-induced liver fibrogenesis and progression in HCV infections. Here, by means of Spike-in SILAC proteomic approach, we first unveiled a specific membrane protein expression signature of HCV cell cultures in the presence of iron overload. Computational analysis of proteomic dataset highlighte…

Liver CirrhosisProteomicshepatitis C virusMaleMESH: Isotope LabelingHSCmedicine.disease_causeBiochemistry0302 clinical medicineFibrosisMESH: Up-RegulationMembrane Proteinhepatic stellate cellliver fibrosishepatic iron overload0303 health sciencesbiologyMESH: ProteomicsMedicine (all)hepatocellular carcinomaBiomedicine; hepatitis c infection; liver fibrosis; hepatic iron overload; vitronectinHepatitis C[SDV.BIBS]Life Sciences [q-bio]/Quantitative Methods [q-bio.QM]Hepatitis CUp-Regulation3. Good healthcell culture-derived HCVIsotope Labeling030220 oncology & carcinogenesisHepatocellular carcinomaBiomedicine; Hepatic iron overload; Hepatitis C infection; Liver fibrosis; Vitronectin; Biomarkers; Cell Line; Hepatitis C; Humans; Iron Overload; Isotope Labeling; Liver Cirrhosis; Male; Membrane Proteins; Proteomics; Up-Regulation; Vitronectin; Molecular Biology; Biochemistry; Medicine (all)HCV[SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/VirologyBiomarker (medicine)VitronectinMESH: Membrane ProteinsMESH: Liver CirrhosisHumanIron OverloadLiver CirrhosiHepatitis C virusvitronectinhepatitis c infectionCell LineMESH: Iron Overload03 medical and health sciencesmedicineHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMolecular Biology030304 developmental biologyMESH: Hepatitis CMESH: HumansMESH: Biological MarkersMembrane ProteinsLiver fibrosiProteomicBiomarkermedicine.diseaseMESH: VitronectinMESH: Maledigestive system diseasesMESH: Cell LineBiomedicineBiomedicine / Abbreviations: HCCHCVccImmunologyCancer researchHepatic stellate cellbiology.proteinSteatosisBiomarkersPROTEOMICS
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Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells

2020

ObjectiveLiver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.DesignThe effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nut…

Liver CirrhosisSTAT3 Transcription Factor0301 basic medicineApoptosisRisk AssessmentSensitivity and SpecificityMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisHepatic Stellate CellsmedicineAnimalsHumansSTAT1610 Medicine & healthSTAT3Cells CulturedLiver injurybiologybusiness.industryRilpivirineFatty liverGastroenterologymedicine.diseaseLiver regenerationLiver RegenerationDisease Models AnimalSTAT1 Transcription FactorTreatment Outcome030104 developmental biology030220 oncology & carcinogenesisbiology.proteinHepatic stellate cellCancer researchbusinessJanus kinase
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Nanotechnology applications for the therapy of liver fibrosis.

2013

Chronic liver diseases represent a major global health problem both for their high prevalence worldwide and, in the more advanced stages, for the limited available curative treatment options. In fact, when lesions of different etiologies chronically affect the liver, triggering the fibrogenesis mechanisms, damage has already occurred and the progression of fibrosis will have a major clinical impact entailing severe complications, expensive treatments and death in end-stage liver disease. Despite significant advances in the understanding of the mechanisms of liver fibrinogenesis, the drugs used in liver fibrosis treatment still have a limited therapeutic effect. Many drugs showing potent ant…

Liver CirrhosisSettore MED/09 - Medicina InternaAntifibrotic drugs CirrhosiLiver fibrosisChemistry PharmaceuticalLiver fibrosisCellPharmacologyBioinformaticsAntifibrotic drugsLiver diseaseNanoparticleHepatic stellate cellsIn vivoFibrosisMedicineNanotechnologyAnimalsHumansTopic HighlightAdverse effectHepatic stellate cellDrug Carriersbusiness.industryTherapeutic effectGastroenterologyLiver fibrosiGeneral Medicinemedicine.diseasemedicine.anatomical_structureNanomedicineTreatment OutcomeCirrhosisHepatic stellate cellNanoparticlesbusinessWorld journal of gastroenterology
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Antifibrotic therapies in the liver.

2015

Significant progress has been made in understanding the principles underlying the development of liver fibrosis. This includes appreciating its dynamic nature, the importance of active fibrolysis in fibrosis regression, and the plasticity of cell populations endowing them with fibrogenic or fibrolytic properties. This is complemented by an increasing array of therapeutic targets with known roles in the progression or regression of fibrosis. With a key role for fibrosis in determining clinical outcomes and encouraging data from recently Food and Drug Administration-approved antifibrotics for pulmonary fibrosis, the development and validation of antifibrotic therapies has taken center stage i…

Liver Cirrhosismedicine.medical_specialtyCirrhosisHepatologyDose titrationCombination therapybusiness.industryLiver fibrosisCell- and Tissue-Based TherapyAngiogenesis InhibitorsHepatologyBioinformaticsmedicine.diseaseArticleFibrosisInternal medicineImmunologyPulmonary fibrosismedicineHepatic stellate cellDisease ProgressionHumansbusinessSeminars in liver disease
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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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Progression of liver fibrosis in post-transplant hepatitis C: mechanisms, assessment and treatment.

2013

SummaryLiver fibrosis results from an excessive wound healing response in most chronic liver diseases, such as hepatitis C. Despite great advances in antiviral therapy in recent years, progressive liver fibrosis remains a major problem for patients with recurrent hepatitis C after liver transplantation. Liver biopsy remains a central tool in the management of HCV-positive liver transplant recipients, but reliable non-invasive methods for the assessment of liver fibrosis, such as ultrasound elastography, are increasingly being incorporated in the management of post-transplant patients, helping predict prognosis, guide treatment decisions, and stratify patients for emerging antifibrotic thera…

Liver Cirrhosismedicine.medical_specialtyCirrhosisMacrophagemedicine.medical_treatmentBiopsyLiver transplantationGastroenterologyAntiviral AgentsPost-transplantFibrosisRecurrenceNAFLDInternal medicineMedicineHumansHepatic stellate cellSerum markerHepatitisTransplantationProgressionHepatologymedicine.diagnostic_testbusiness.industryT cellSecond hitHepatitis Cmedicine.diseasePrognosisFibrosisHepatitis CLiver TransplantationTransplantationCirrhosisLiverTGFbetaLiver biopsyHCVHepatic stellate cellDisease ProgressionInterferonElasticity Imaging TechniquesCollagenAntifibroticElastographybusinessJournal 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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Induced pluripotent stem cells in liver disease

2021

Abstract The development of suitable and reproducible liver cell models is fundamental for regenerative medicine, drug screening, and disease modeling. Human primary hepatocytes are the gold standard not only for hepatic cell therapy but also for preclinical toxicological screening or the study of liver disease; however, their limited availability, variability, and phenotypic instability hamper their use. Recent advances in stem cell technology have allowed the generation of induced pluripotent stem cells (iPSCs) from different somatic cell types and their differentiation into hepatocyte-like cells (HLCs), which can provide unlimited cell source for their use in hepatology studies. We revie…

Liver diseasemedicine.anatomical_structureSomatic cellLiver cellCellCancer researchmedicineHepatic stellate cellStem cellBiologymedicine.diseaseInduced pluripotent stem cellRegenerative medicine
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385 MOLECULAR STAGES OF PDGFB DRIVEN LIVER FIBROSIS: LESONS FROM A TRANSGENIC MOUSE MODEL

2012

underlying pathomechanisms is hampered by the lack of a suitable animal model. To circumvent this problem, we studied hepcidinknockout (KO) mice as a model of iron-overload associated liver disease. Methods: 6 and 12 month-old hepcidin-KO and -wild type (WT) mice fed 3% iron carbonyl-containing diet (Fe-diet) since four weeks of age were compared to age-matched WT and KO animals kept on standard diet. The liver phenotype was quantified serologically as well as morphometrically based on hematoxylin & eosin, Prussian blue and Sirius red stainings. Liver iron content was determined by atomic mass absorption. Liver fibrosis development was determined by collagen RT-PCR and hydroxyproline assay.…

Liver injuryPathologymedicine.medical_specialtyHepatologymedicine.diagnostic_testbiologyH&E stainmedicine.diseaseHepatic stellate cell activationHydroxyprolinechemistry.chemical_compoundLiver diseaseEndocrinologychemistryHepcidinInternal medicineSerum ironmedicinebiology.proteinSirius RedJournal of Hepatology
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