0000000000347753

AUTHOR

Carmine Mancone

showing 9 related works from this author

Additional file 1: of CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA

2015

(a) Characterization of isolated exosomes. Left panel: DSL for exosomes released by SKHep Middle panel: Western blot forTsg101 and HSC70 in SkHep cells and their relative exosomes. Right panel: Confocal microscopy analysis on HUVECs treated for 1, 3 and 6 hours with 5 mg/ml of SKHep-derived exosomes. HUVECs were stained with phalloidin Alexa Fluor (green), nuclear counterstaining was performed using DAPI (blue), exosomes were labelled with PKH26 (red). (b) Target analysis. Real time-PCR analysis on HUVECs treated for 18 h with 5 mg/ml of SkHep-derived exosomes. Normalized for b-actin the DDct were indicated as fold of induction respect to control (untreated cells). *p<0.05. (c) Tubulogen…

embryonic structures
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Evidence for a common progenitor of epithelial and mesenchymal components of the liver

2013

Tissues of the adult organism maintain the homeostasis and respond to injury by means of progenitor/stem cell compartments capable to give rise to appropriate progeny. In organs composed by histotypes of different embryological origins (e.g. The liver), the tissue turnover may in theory involve different stem/precursor cells able to respond coordinately to physiological or pathological stimuli. In the liver, a progenitor cell compartment, giving rise to hepatocytes and cholangiocytes, can be activated by chronic injury inhibiting hepatocyte proliferation. The precursor compartment guaranteeing turnover of hepatic stellate cells (HSCs) (perisinusoidal cells implicated with the origin of the …

Cellular differentiationLiver Stem CellDesminMice0302 clinical medicineMESH: AnimalsMESH: Nerve Tissue ProteinsHepatic stellate cellCells Cultured0303 health sciencesMesenchymal Stromal CellStem CellsCell DifferentiationCell biologyEndothelial stem cellMESH: DesminMESH: Models AnimalLiverMESH: Epithelial CellsDifferentiationModels Animal030211 gastroenterology & hepatologyStem cellMESH: Stem Cell Transplantationhepatic stellate cell; cell transplantation; liver stem cell; differentiationMESH: Cells CulturedMESH: Cell DifferentiationCell transplantation; Differentiation; Hepatic stellate cell; Liver stem cell; Animals; Cell Differentiation; Cell Line; Cell Lineage; Cell Proliferation; Cells Cultured; Desmin; Epithelial Cells; Glial Fibrillary Acidic Protein; In Vitro Techniques; Liver; Mesenchymal Stromal Cells; Mice; Mice Nude; Models Animal; Nerve Tissue Proteins; Stem Cell Transplantation; Stem Cells; Cell Biology; Molecular BiologyClinical uses of mesenchymal stem cellsMice NudeNerve Tissue ProteinsMESH: Stem Cells[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyIn Vitro TechniquesCell Line03 medical and health sciencesStem CellMESH: Cell ProliferationGlial Fibrillary Acidic ProteinMESH: Mice NudeAnimalsCell LineageProgenitor cellMESH: MiceMolecular Biology030304 developmental biologyCell ProliferationOriginal PaperEpithelial CellAnimalIn Vitro TechniqueMesenchymal stem cellEpithelial CellsMesenchymal Stem CellsCell BiologyMESH: Cell LineageMESH: Cell LineLiver stem cellNerve Tissue ProteinHepatic stellate cellMESH: Mesenchymal Stromal CellsCell transplantationMESH: LiverStem Cell Transplantation
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MiR675-5p Acts on HIF-1α to Sustain Hypoxic Responses: A New Therapeutic Strategy for Glioma

2016

Hypoxia is a common feature in solid tumours. In glioma, it is considered the major driving force for tumour angiogenesis and correlates with enhanced resistance to conventional therapies, increased invasiveness and a poor prognosis for patients. Here we describe, for the first time, that miR675-5p, embedded in hypoxia-induced long non-coding RNA H19, plays a mandatory role in establishing a hypoxic response and in promoting hypoxia-mediated angiogenesis. We demonstrated, in vitro and in vivo, that miR675-5p over expression in normoxia is sufficient to induce a hypoxic moreover, miR675-5p depletion in low oxygen conditions, drastically abolishes hypoxic responses including angiogenesis. In …

0301 basic medicinemiRNA675AngiogenesisMedicine (miscellaneous)RNA-binding proteinAngiogenesis; Glioma; HuR; Hypoxia; miRNA675; Optical imaging; VHL; Medicine (miscellaneous); Pharmacology Toxicology and Pharmaceutics (miscellaneous)BiologyToxicology and Pharmaceutics (miscellaneous)Cell LineELAV-Like Protein 1Miceoptical imaging03 medical and health sciencesSettore BIO/13 - Biologia ApplicataStress PhysiologicalIn vivoVHLGliomamicroRNAmedicineAnimalsHumansPharmacology Toxicology and Pharmaceutics (miscellaneous)PharmacologyAngiogenesis; HuR; VHL.; glioma; hypoxia; miRNA675; optical imagingMessenger RNANeovascularization PathologichypoxiaVHL.RNAGliomaHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.disease3. Good healthAngiogenesiMicroRNAs030104 developmental biologyImmunologyCancer researchHeterograftsHuRAngiogenesismedicine.symptomResearch PaperTheranostics
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The stable repression of mesenchymal program is required for hepatocyte identity: A novel role for hepatocyte nuclear factor 4α

2011

The concept that cellular terminal differentiation is stably maintained once development is complete has been questioned by numerous observations showing that differentiated epithelium may undergo an epithelial-to-mesenchymal transition (EMT) program. EMT and the reverse process, mesenchymal-to-epithelial transition (MET), are typical events of development, tissue repair, and tumor progression. In this study, we aimed to clarify the molecular mechanisms underlying these phenotypic conversions in hepatocytes. Hepatocyte nuclear factor 4α (HNF4α) was overexpressed in different hepatocyte cell lines and the resulting gene expression profile was determined by real-time quantitative polymerase…

Transcription FactorCellular differentiationMESH: Mice KnockoutMESH: HepatocytesMesodermMice0302 clinical medicineMESH: Liver NeoplasmsMESH: AnimalsHepatocyteHepatocyte Nuclear Factor 1-alphaMESH: Carcinoma HepatocellularRegulator geneHepatocyte differentiationMice KnockoutMESH: Mesoderm0303 health sciencesLiver NeoplasmsCell DifferentiationMESH: Transcription FactorsCell biologyHepatocyte nuclear factorsPhenotypeMESH: Models AnimalHepatocyte Nuclear Factor 4MESH: Epithelial CellsLiver Neoplasm030220 oncology & carcinogenesisModels AnimalMESH: Hepatocyte Nuclear Factor 4HumanMESH: Cell DifferentiationMESH: Cell Line TumorCarcinoma Hepatocellular[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyMESH: PhenotypeArticle03 medical and health scienceshepatocyte; mesenchymal program; SnailCell Line TumorAnimalsHumansMESH: Hepatocyte Nuclear Factor 1-alphaMESH: MiceTranscription factorAnimals; Carcinoma Hepatocellular; Cell Differentiation; Cell Line Tumor; Epithelial Cells; Hepatocyte Nuclear Factor 1-alpha; Hepatocyte Nuclear Factor 4; Hepatocytes; Humans; Liver Neoplasms; Mesoderm; Mice; Mice Knockout; Models Animal; Phenotype; Snail Family Transcription Factors; Transcription Factors; Hepatology030304 developmental biologyEpithelial CellMESH: HumansHepatologyAnimalMesenchymal stem cellEpithelial CellsSnail Family Transcription FactorMolecular biologyHepatocyte nuclear factor 4HepatocytesSnail Family Transcription FactorsChromatin immunoprecipitationTranscription Factors
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Data on the effects of low iron diet on serum lipid profile in HCV transgenic mouse model

2017

Here, we presented new original data on the effects of iron depletion on the circulating lipid profile in B6HCV mice, a murine model of HCV-related dyslipidemia. Male adult B6HCV mice were subjected to non-invasive iron depletion by low iron diet. Serum iron concentration was assessed for evaluating the effects of the dietary iron depletion. Concentrations of circulating triglycerides, total cholesterol, Low Density Lipoproteins (LDLs), High Density Lipoproteins (HDLs) were analyzed and reported by using stacked line charts. The present data indicated that low serum iron concentration is associated to i) lower serum triglycerides concentrations and ii) increased circulating LDLs. The presen…

0301 basic medicineGenetically modified mousemedicine.medical_specialtyLow density lipoproteins3304High densityLow density lipoproteinlcsh:Computer applications to medicine. Medical informaticsTriglyceride03 medical and health sciences0302 clinical medicineInternal medicinemedicineIron depletion; Low density lipoproteins; Triglycerides; 3304; MultidisciplinarySerum triglycerideslcsh:Science (General)TriglyceridesData ArticleDietary ironMultidisciplinarymedicine.diagnostic_testChemistrymedicine.diseaseIron depletion030104 developmental biologyEndocrinologyBiochemistrySerum ironlcsh:R858-859.7030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)Lipid profileDyslipidemiaIron depletionlcsh:Q1-390Data in Brief
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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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CD90+ liver cancer cells modulate endothelial cell phenotype through the release of exosomes containing H19 lncRNA

2015

Background CD90+ liver cancer cells have been described as cancer stem-cell-like (CSC), displaying aggressive and metastatic phenotype. Using two different in vitro models, already described as CD90+ liver cancer stem cells, our aim was to study their interaction with endothelial cells mediated by the release of exosomes. Methods Exosomes were isolated and characterized from both liver CD90+ cells and hepatoma cell lines. Endothelial cells were treated with exosomes, as well as transfected with a plasmid containing the full length sequence of the long non-coding RNA (lncRNA) H19. Molecular and functional analyses were done to characterize the endothelial phenotype after treatments. Results …

Cancer ResearchAngiogenesisAngiogenesis; CD90+ liver cancer cells; Exosomes; Long-non-coding RNA H19; Antigens Thy-1; Cell Adhesion; Cell Line Tumor; Endothelial Cells; Exosomes; Human Umbilical Vein Endothelial Cells; Humans; Liver Neoplasms; RNA Long Noncoding; Phenotype; Molecular Medicine; Oncology; Cancer ResearchBiologyCD90+ liver cancer cellsExosomesCell LineSettore BIO/13 - Biologia ApplicataCancer stem cellCell Line TumormedicineCell AdhesionHuman Umbilical Vein Endothelial CellsHumansCD90AntigensThy-1TumorExosomes Long-non-coding RNA H19 CD90+ liver cancer cells AngiogenesisResearchLiver NeoplasmsCancerEndothelial Cellsmedicine.diseaseMicrovesiclesCell biologyEndothelial stem cellPhenotypeOncologyembryonic structuresThy-1 AntigensRNAMolecular MedicineRNA Long NoncodingLong NoncodingAngiogenesisStem cellLiver cancerLong-non-coding RNA H19Molecular Cancer
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SILAC labeling coupled to shotgun proteomics analysis of membrane proteins of liver stem/hepatocyte allows to candidate the inhibition of TGF-beta pa…

2014

Background: Despite extensive research on hepatic cells precursors and their differentiated states, much remains to be learned about the mechanism underlying the self-renewal and differentiation.Results: We apply the SILAC (stable isotope labeling by amino acids in cell culture) approach to quantitatively compare the membrane proteome of the resident liver stem cells (RLSCs) and their progeny spontaneously differentiated into epithelial/hepatocyte (RLSCdH). By means of nanoLC-MALDI-TOF/TOF approach, we identified and quantified 248 membrane proteins and 57 of them were found modulated during hepatocyte differentiation. Functional clustering of differentially expressed proteins by Ingenuity …

Hepatocyte differentiationProteomicsStem cellChemistryResearchLiver Stem CellProteomicProteomicsBioinformaticsBiochemistrySILACCell biologyMembrane proteinStable isotope labeling by amino acids in cell cultureTGF beta signaling pathwayHepatocyte; Proteomics; SILAC; Stem cell; Biochemistry; Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyHepatocyteStem cellShotgun proteomics[SDV.BDD]Life Sciences [q-bio]/Development BiologyMolecular BiologyProteome Science
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Extracellular Matrix Molecular Remodeling in Human Liver Fibrosis Evolution

2016

Chronic liver damage leads to pathological accumulation of ECM proteins (liver fibrosis). Comprehensive characterization of the human ECM molecular composition is essential for gaining insights into the mechanisms of liver disease. To date, studies of ECM remodeling in human liver diseases have been hampered by the unavailability of purified ECM. Here, we developed a decellularization method to purify ECM scaffolds from human liver tissues. Histological and electron microscopy analyses demonstrated that the ECM scaffolds, devoid of plasma and cellular components, preserved the three-dimensional ECM structure and zonal distribution of ECM components. This method has been then applied on 57 l…

Liver Cirrhosis0301 basic medicineProteomicsPathologyProteomeBiopsylcsh:MedicineHepacivirusMatrix (biology)ProteomicsBiochemistryExtracellular matrixMiceLiver disease0302 clinical medicineFibrosisSettore BIO/13 - Biologia ApplicataMedicine and Health Scienceslcsh:Scienceliver fibrosisExtracellular Matrix ProteinsMultidisciplinaryDecellularizationAnimals; Extracellular Matrix; Hepacivirus; Humans; Liver; Liver Cirrhosis; Mice; Proteome; Proteomics; Tissue Scaffolds; Disease ProgressionTissue ScaffoldsChemistryLiver DiseasesLiver030220 oncology & carcinogenesisProteomeDisease ProgressionCellular Structures and OrganellesAnatomyliver fibrosis; extracellular matrix; proteomicsResearch Articlemedicine.medical_specialtyHistologySettore BIO/06extracellular matrixSurgical and Invasive Medical ProceduresGastroenterology and HepatologyScaffold03 medical and health sciencesmedicineAnimalsHumansHuman liverlcsh:RBiology and Life SciencesProteinsCell Biologymedicine.diseaseFibrosisLiver Fibrosi030104 developmental biologyLiver Fibrosis; Scaffold; Proteomicslcsh:QCollagensDevelopmental Biology
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