Search results for "Stellate cell"

showing 10 items of 106 documents

Understanding the implication of autophagy in the activation of hepatic stellate cells in liver fibrosis: are we there yet?

2021

Liver fibrosis (LF) occurs as a result of persistent liver injury and can be defined as a pathologic, chronic, wound-healing process in which functional parenchyma is progressively replaced by fibrotic tissue. As a phenomenon involved in the majority of chronic liver diseases, and therefore prevalent, it exerts a significant impact on public health. This impact becomes even more patent given the lack of a specific pharmacological therapy, with LF only being ameliorated or prevented through the use of agents that alleviate the underlying causes. Hepatic stellate cells (HSCs) are fundamental mediators of LF, which, activated in response to pro-fibrotic stimuli, transdifferentiate from a quies…

0301 basic medicineLiver injuryLiver CirrhosisProgrammed cell deathCell cycle checkpointbusiness.industryAutophagymedicine.diseasePathology and Forensic Medicine03 medical and health sciences030104 developmental biology0302 clinical medicineCell culture030220 oncology & carcinogenesisLipid dropletCancer researchHepatic stellate cellmedicineAutophagyHepatic Stellate CellsAnimalsHumansbusinessMyofibroblastThe Journal of pathologyReferences
researchProduct

Silencing of hepatic fate-conversion factors induce tumorigenesis in reprogrammed hepatic progenitor-like cells

2016

Abstract Background Several studies have reported the direct conversion of mouse fibroblasts to hepatocyte-like cells with different degrees of maturation by expression of hepatic fate-conversion factors. Methods We have used a combination of lentiviral vectors expressing hepatic fate-conversion factors with Oct4, Sox2, Klf4, and Myc to convert mouse embryonic fibroblasts into hepatic cells. Results We have generated hepatic cells with progenitor-like features (iHepL cells). iHepL cells displayed basic hepatocyte functions but failed to perform functions characteristic of mature hepatocytes such as significant Cyp450 or urea cycle activities. iHepL cells expressed multiple hepatic-specific …

0301 basic medicineMaleCarcinogenesisCellular differentiationMedicine (miscellaneous)Gene ExpressionReceptors G-Protein-CoupledMiceMice Inbred NODHepatocyteTransgenesStem CellsTeratomaCell DifferentiationForkhead Transcription FactorsCellular ReprogrammingCell biologyKLF4Molecular MedicineStem cellReprogrammingDirect reprogrammingGenetic VectorsKruppel-Like Transcription FactorsBiologyBiochemistry Genetics and Molecular Biology (miscellaneous)Proto-Oncogene Proteins c-myc03 medical and health sciencesKruppel-Like Factor 4SOX2AnimalsHepatectomyGene SilencingProgenitor cellResearchXenograftSOXB1 Transcription FactorsLentivirusCD24 AntigenCell BiologyFibroblastsEmbryo MammalianEmbryonic stem cell030104 developmental biologyTumorigenesisHepatic stellate cellHepatocytesOctamer Transcription Factor-3BiomarkersProgenitorStem Cell Research & Therapy
researchProduct

Evaluating the antifibrotic potency of galunisertib in a human ex vivo model of liver fibrosis

2017

Background and Purpose Liver fibrosis is a major cause of liver-related mortality and, so far, no effective antifibrotic drug is available. Galunisertib, a TGF-β receptor type I kinase inhibitor, is a potential candidate for the treatment of liver fibrosis. Here, we evaluated the potency of galunisertib in a human ex vivo model of liver fibrosis. Experimental Approach Antifibrotic potency and associated mechanisms were studied ex vivo, using both healthy and cirrhotic human precision-cut liver slices. Fibrosis-related parameters, both transcriptional and translational level, were assessed after treatment with galunisertib. Key Results Galunisertib showed a prominent antifibrotic potency. Ph…

0301 basic medicinePharmacologymedicine.medical_specialtyPharmacologyBiologyExtracellular matrix03 medical and health sciences030104 developmental biology0302 clinical medicineEndocrinologyMechanism of action030220 oncology & carcinogenesisInternal medicinemedicineHepatic stellate cellGalunisertibPotencymedicine.symptomSignal transductionReceptorEx vivoBritish Journal of Pharmacology
researchProduct

Fasting inhibits hepatic stellate cells activation and potentiates anti-cancer activity of Sorafenib in hepatocellular cancer cells

2017

BACKGROUND: Hepatocellular carcinoma (HCC) has a poor outcome. Most HCCs develop in the context of liver fibrosis and cirrhosis caused by chronic inflammation. Short-term fasting approaches enhance the activity of chemotherapy in preclinical cancer models, other than HCC. Multi-tyrosine kinase inhibitor Sorafenib is the mainstay of treatment in HCC. However, its benefit is frequently short-lived. Whether fasting can alleviate liver fibrosis and whether combining fasting with Sorafenib is beneficial remains unknown. METHODS: 24 hour fasting (2% serum, 0.1% glucose)-induced changes on human hepatic stellate cells (HSC) LX-2 proliferation/viability/cell cycle were assessed by MTT and flow cyto…

0301 basic medicineSorafenibLipopolysaccharidesNiacinamidemedicine.medical_specialtyCirrhosisCarcinoma HepatocellularTime FactorsPhysiologyGlucose uptakeClinical BiochemistryAntineoplastic AgentsLiver Cirrhosis Experimental03 medical and health sciencesFibrosisNon-alcoholic Fatty Liver DiseaseInternal medicineSorafenib fastingmedicineHepatic Stellate CellsAnimalsHumansneoplasmsCell Proliferationhepatic stellate cellDose-Response Relationship Drugbusiness.industryMedicine (all)Phenylurea CompoundsLiver NeoplasmsCancerCell BiologyFastingHep G2 Cellshepatocellular carcinomaSorafenibmedicine.diseasedigestive system diseasesGene Expression Regulation NeoplasticMice Inbred C57BL030104 developmental biologyEndocrinologyGlucoseHepatocellular carcinomaHepatic stellate cellCancer researchSteatohepatitisbusinessmedicine.drug
researchProduct

Three-Dimensional Spheroid Primary Human Hepatocytes in Monoculture and Coculture with Nonparenchymal Cells

2018

Recent advances in the development of various culture platforms are promising for achieving more physiologically relevant in vitro hepatic models using primary human hepatocytes (PHHs). Previous studies have shown the value of PHHs three-dimensional (3D) spheroid models, cultured in low cell number (1330-2000 cells/3D spheroid), to study long-term liver function as well as pharmacological drug effects and toxicity. In this study, we report that only plateable PHHs aggregate and form compact 3D spheroids with a success rate of 79%, and 96% reproducibility. Out of 3D spheroid forming PHH lots, 65% were considered stable (<50% ATP decrease) over the subsequent 14 days of culture, with reproduc…

0301 basic medicineTime FactorsCell SurvivalKupffer CellsCellCell Culture TechniquesBiomedical EngineeringMedicine (miscellaneous)BioengineeringCell SeparationCryopreservation03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSpheroids CellularmedicineHumansRNA MessengerCell ShapeCell AggregationCell SizeCryopreservationChemistrySpheroidAlbuminCoculture TechniquesIn vitroCell biology030104 developmental biologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisHepatocytesHepatic stellate cellLiver functionBiomarkersImmunostainingTissue Engineering Part C: Methods
researchProduct

Human Upcyte Hepatocytes: Characterization of the Hepatic Phenotype and Evaluation for Acute and Long-Term Hepatotoxicity Routine Testing

2016

The capacity of human hepatic cell-based models to predict hepatotoxicity depends on the functional performance of cells. The major limitations of human hepatocytes include the scarce availability and rapid loss of the hepatic phenotype. Hepatoma cells are readily available and easy to handle, but are metabolically poor compared with hepatocytes. Recently developed human upcyte hepatocytes offer the advantage of combining many features of primary hepatocytes with the unlimited availability of hepatoma cells. We analyzed the phenotype of upcyte hepatocytes comparatively with HepG2 cells and adult primary human hepatocytes to characterize their functional features as a differentiated hepatic …

0301 basic medicineTime FactorsPrimary Cell CultureTransfectionToxicologyRisk AssessmentTranscriptome03 medical and health sciences0302 clinical medicineMetabolomicsCytochrome P-450 Enzyme SystemIn vivoToxicity TestsmedicineHumansChildGlycogen synthaseDose-Response Relationship DrugbiologyInfant NewbornCytochrome P450Hep G2 CellsMiddle Agedmedicine.diseasePhenotypeHigh-Throughput Screening AssaysIsoenzymesOxidative StressPhenotype030104 developmental biologyGene Expression RegulationLiver030220 oncology & carcinogenesisHepatocytesbiology.proteinHepatic stellate cellCancer researchChemical and Drug Induced Liver InjurySteatosisTranscriptomeToxicological Sciences
researchProduct

Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
researchProduct

The Unfolded Protein Response Plays a Predominant Homeostatic Role in Response to Mitochondrial Stress in Pancreatic Stellate Cells.

2016

Activated pancreatic stellate cells (PaSC) are key participants in the stroma of pancreatic cancer, secreting extracellular matrix proteins and inflammatory mediators. Tumors are poorly vascularized, creating metabolic stress conditions in cancer and stromal cells that necessitate adaptive homeostatic cellular programs. Activation of autophagy and the endoplasmic reticulum unfolded protein response (UPR) have been described in hepatic stellate cells, but the role of these processes in PaSC responses to metabolic stress is unknown. We reported that the PI3K/mTOR pathway, which AMPK can regulate through multiple inputs, modulates PaSC activation and fibrogenic potential. Here, using primary a…

0301 basic medicinelcsh:MedicineApoptosisMitochondrionAMP-Activated Protein KinasesEndoplasmic ReticulumBiochemistrychemistry.chemical_compoundMiceeIF-2 KinasePhosphatidylinositol 3-Kinases0302 clinical medicineFluorescence MicroscopyCell SignalingTumor Microenvironment2.1 Biological and endogenous factorsSmall interfering RNAsAetiologylcsh:ScienceEnergy-Producing OrganellesCancerMice KnockoutMicroscopyMultidisciplinarySecretory PathwayCell DeathTOR Serine-Threonine KinasesLight MicroscopySignaling CascadesCell biologyMitochondriaNeoplasm ProteinsUp-RegulationNucleic acidsCell Processes030220 oncology & carcinogenesisCellular Structures and OrganellesResearch ArticleSignal TransductionProgrammed cell deathCell PhysiologyGeneral Science & TechnologyAutophagic Cell DeathKnockoutBiologyBioenergeticsResearch and Analysis MethodsStress Signaling Cascade03 medical and health sciencesGeneticsAutophagyAnimalsNon-coding RNAPancreasPI3K/AKT/mTOR pathwaylcsh:RAutophagyAMPKBiology and Life SciencesCell BiologyCell MetabolismGene regulationPancreatic NeoplasmsEnzyme Activation030104 developmental biologychemistryHepatic stellate cellUnfolded protein responseUnfolded Protein ResponseRNAlcsh:QGene expressionInterleukin-4Digestive DiseasesRottlerinTranscription Factor CHOP
researchProduct

Centrosome amplification mediates small extracellular vesicles secretion via lysosome disruption

2020

SummaryBidirectional communication between cells and their surrounding environment is critical in both normal and pathological settings. Extracellular vesicles (EVs), which facilitate the horizontal transfer of molecules between cells, are recognized as an important constituent of cell-cell communication. In cancer, alterations in EV secretion contribute to the growth and metastasis of tumor cells. However, the mechanisms underlying these changes remain largely unknown. Here, we show that centrosome amplification is associated with and sufficient to promote small extracellular vesicle (SEV) secretion in pancreatic cancer cells. This is a direct result due of lysosomal dysfunction, caused by…

0303 health sciencesChemistry[SDV]Life Sciences [q-bio]Extracellular vesicle[SDV.BC]Life Sciences [q-bio]/Cellular Biologymedicine.diseaseMetastasisCell biology03 medical and health sciences0302 clinical medicinemedicine.anatomical_structureCentrosome030220 oncology & carcinogenesisPancreatic cancerLysosomeCancer cellmedicineHepatic stellate cellSecretion030304 developmental biology
researchProduct

Expression of glial filament protein (GFP) in nerve sheaths and non-neural cells re-examined using monoclonal antibodies, with special emphasis on th…

1986

We describe two novel monoclonal antibodies specific for glial filament protein (GFP), i.e., GF12.23 and GF12.24 (both IgG2a]. These cross-react over a broad range of species with epitopes located in the alpha-helical rod domain typical of all intermediate filament (IF) proteins. These monoclonal antibodies were used, in conjunction with other monoclonal GFP antibodies, rabbit antiserum to GFP, and various antibodies to other cytoskeletal proteins, to examine the occurrence of GFP in cells outside of the central nervous system of rodents, cows, and humans. We detected some scattered GFP-containing cells in the neural sheaths in some species but not in others, and we obtained different resul…

AdenomaCancer Researchmedicine.drug_classGuinea PigsAdenoma PleomorphicFluorescent Antibody TechniqueCross ReactionsMonoclonal antibodyEyeEpitopeEpitheliumSalivary GlandsGreen fluorescent proteinEpitopesSpecies SpecificityGlial Fibrillary Acidic ProteinmedicineAnimalsHumansVimentinIntermediate filamentMolecular BiologyMyelin SheathbiologyMyoepithelial cellAntibodies MonoclonalCell BiologyMolecular biologyRatsMicroscopy FluorescenceMonoclonalImmunologybiology.proteinHepatic stellate cellKeratinsCattleAntibodyDevelopmental BiologyDifferentiation; research in biological diversity
researchProduct