0000000000022537

AUTHOR

Gianluigi Mazzoccoli

0000-0003-3535-7635

showing 9 related works from this author

Mutual Antagonism between Circadian Protein Period 2 and Hepatitis C Virus Replication in Hepatocytes

2013

BackgroundHepatitis C virus (HCV) infects approximately 3% of the world population and is the leading cause of liver disease, impacting hepatocyte metabolism, depending on virus genotype. Hepatic metabolic functions show rhythmic fluctuations with 24-h periodicity (circadian), driven by molecular clockworks ticking through translational-transcriptional feedback loops, operated by a set of genes, called clock genes, encoding circadian proteins. Disruption of biologic clocks is implicated in a variety of disorders including fatty liver disease, obesity and diabetes. The relation between HCV replication and the circadian clock is unknown.MethodsWe investigated the relationship between HCV core…

MaleGastroenterology and hepatologyCircadian clockHepacivirusVirus ReplicationHepatitisMolecular cell biologyCellular Stress ResponsesMultidisciplinaryViral Core ProteinsQMechanisms of Signal TransductionRPeriod Circadian ProteinsMiddle AgedHepatitis CCLOCKPER2ARNTLInfectious hepatitisLiverMedicineInfectious diseasesRNA ViralFemaleResearch ArticleSignal TransductionPER1AdultHistologyFeedback RegulationGenotypeSciencePeriod (gene)DNA transcriptionViral diseasesGenome ViralBiologyCell LineCell Line TumorGeneticsHumansBiologyLiver diseasesAgedVirologyHepatocytesPeriod Circadian ProteinsGene expressionARNTL2PLoS ONE
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Amphiregulin activates human hepatic stellate cells and is upregulated in non alcoholic steatohepatitis

2015

AbstractAmphiregulin (AR) involvement in liver fibrogenesis and hepatic stellate cells (HSC) regulation is under study. Non-alcoholic fatty liver disease (NAFLD) and its more severe form non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular cancer (HCC). Our aim was to investigate ex vivo the effect of AR on human primary HSC (hHSC) and verify in vivo the relevance of AR in NAFLD fibrogenesis. hHSC isolated from healthy liver segments were analyzed for expression of AR and its activator, TNF-α converting enzyme (TACE). AR induction of hHSC proliferation and matrix production was estimated in the presence of antagonists. AR involvement in fibrogenesis was also ass…

medicine.medical_specialtyBiopsyGene ExpressionADAM17 ProteinBiologyAmphiregulinSeverity of Illness Indexp38 Mitogen-Activated Protein Kinasesdigestive systemArticleMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineDownregulation and upregulationAmphiregulinGrowth factor receptorNon-alcoholic Fatty Liver DiseaseInternal medicineHepatic Stellate CellsmedicineAnimalsHumansProtein Kinase CPI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesMultidisciplinaryFatty livernutritional and metabolic diseasesmedicine.diseaseFibrosisActinsdigestive system diseases3. Good healthEnzyme ActivationErbB ReceptorsADAM ProteinsDisease Models AnimalEndocrinologyHepatic stellate cellCancer research030211 gastroenterology & hepatologyTumor necrosis factor alphaCollagenSteatohepatitisSignal TransductionScientific Reports
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DNA Hypomethylation and Histone Variant macroH2A1 Synergistically Attenuate Chemotherapy-Induced Senescence to Promote Hepatocellular Carcinoma Progr…

2016

Abstract Aging is a major risk factor for progression of liver diseases to hepatocellular carcinoma (HCC). Cellular senescence contributes to age-related tissue dysfunction, but the epigenetic basis underlying drug-induced senescence remains unclear. macroH2A1, a variant of histone H2A, is a marker of senescence-associated heterochromatic foci that synergizes with DNA methylation to silence tumor-suppressor genes in human fibroblasts. In this study, we investigated the relationship between macroH2A1 splice variants, macroH2A1.1 and macroH2A1.2, and liver carcinogenesis. We found that protein levels of both macroH2A1 isoforms were increased in the livers of very elderly rodents and humans, a…

0301 basic medicineEpigenomicsCHROMATINCancer ResearchLIVERCancer Research; OncologyGene ExpressionSECRETORY PHENOTYPEHCV CORE PROTEINHistonesCell MovementProtein IsoformsCellular SenescenceEpigenomicsAged 80 and overMice KnockoutbiologyLiver NeoplasmsMETHYLATIONHep G2 CellsCANCERChromatinHistoneOncologyDNA methylationAzacitidineDisease ProgressionCell agingSTEM-CELLSSenescenceAdultEXPRESSIONCarcinoma HepatocellularArticle5-AZA-2'-DEOXYCYTIDINE03 medical and health sciencesCell Line TumorAnimalsHumansEpigeneticsCell ProliferationDNA Methylationbeta-GalactosidaseMolecular biologyMice Inbred C57BLMICE030104 developmental biologybiology.proteinCancer researchDNA hypomethylation
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Extracellular Superoxide Dismutase Expression in Papillary Thyroid Cancer Mesenchymal Stem/Stromal Cells Modulates Cancer Cell Growth and Migration

2017

AbstractTumor stroma-secreted growth factors, cytokines, and reactive oxygen species (ROS) influence tumor development from early stages to the metastasis phase. Previous studies have demonstrated downregulation of ROS-producing extracellular superoxide dismutase (SOD3) in thyroid cancer cell lines although according to recent data, the expression of SOD3 at physiological levels stimulates normal and cancer cell proliferation. Therefore, to analyze the expression of SOD3 in tumor stroma, we characterized stromal cells from the thyroid. We report mutually exclusive desmoplasia and inflammation in papillary and follicular thyroid cancers and the presence of multipotent mesenchymal stem/stroma…

0301 basic medicineendocrine systemPathologymedicine.medical_specialtyStromal cellendocrine system diseasesThyroid GlandBiologyArticleMetastasisPapillary thyroid cancer03 medical and health sciences0302 clinical medicineCell MovementExtracellular ;Thyroid ;Cancer ;Cell .Adenocarcinoma FollicularParacrine CommunicationBiomarkers TumormedicineHumansThyroid NeoplasmsThyroid cancerCell ProliferationMultidisciplinarySuperoxide DismutaseMesenchymal stem cellThyroidEpithelial CellsMesenchymal Stem Cellsmedicine.diseaseFibrosisCarcinoma PapillaryDesmoplasiaGene Expression Regulation NeoplasticPhenotype030104 developmental biologymedicine.anatomical_structureThyroid Cancer Papillary030220 oncology & carcinogenesisCancer cellmedicine.symptomExtracellular SpaceScientific Reports
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Immunopositivity for histone macroH2A1 isoforms marks steatosisassociated hepatocellular carcinoma.

2012

BackgroundHepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Prevention and risk reduction are important and the identification of specific biomarkers for early diagnosis of HCC represents an active field of research. Increasing evidence indicates that fat accumulation in the liver, defined as hepatosteatosis, is an independent and strong risk factor for developing an HCC. MacroH2A1, a histone protein generally associated with the repressed regions of chromosomes, is involved in hepatic lipid metabolism and is present in two alternative spliced isoforms, macroH2A1.1 and macroH2A1.2. These isoforms have been shown to predict lung and colon cancer recurrence but to ou…

MalePathologyMouseBiological Markers/metabolismEpidemiologyTumor Microenvironment/geneticsColorectal cancerGene ExpressionHepatocytes/metabolism/pathologyNonalcoholic SteatohepatitisHistonesFatty Liver/chemically induced/complications/genetics/metabolismMice0302 clinical medicineGastrointestinal CancersTumor MicroenvironmentPathologyProtein IsoformsDiethylnitrosamineSettore MED/49 - Scienze Tecniche Dietetiche ApplicateMice KnockoutRegulation of gene expression0303 health sciencesMultidisciplinaryProtein Isoforms/genetics/metabolismbiologyLiver DiseasesPTEN Phosphohydrolase/deficiency/geneticshepatocellular carcinoma biomarker histone variant steatosis epigeneticsLiver NeoplasmsQFatty liverRHistone ModificationAnimal ModelsImmunohistochemistry3. Good healthHistoneOncology030220 oncology & carcinogenesisHepatocellular carcinomaMedicineEpigeneticsCarcinoma Hepatocellular/etiology/genetics/metabolism/pathologyResearch ArticleGene isoformmedicine.medical_specialtyCarcinoma HepatocellularHistologyClinical Research DesignScienceGastroenterology and HepatologyDiet High-Fat03 medical and health sciencesModel OrganismsDiagnostic MedicineGastrointestinal TumorsGeneticsCancer GeneticsCancer Detection and DiagnosisEarly DetectionmedicineAnimalsHumansAnimal Models of DiseaseObesityddc:612BiologyHistones/genetics/metabolismNutrition030304 developmental biologyCell NucleusCell Nucleus/genetics/metabolism/pathologyTumor microenvironmentbusiness.industryPTEN PhosphohydrolaseCancers and NeoplasmsHepatocellular Carcinomamedicine.diseasedigestive system diseasesFatty LiverBiomarker EpidemiologyGene Expression RegulationHepatocytesbiology.proteinLiver Neoplasms/etiology/genetics/metabolism/pathologySteatosisbusinessBiomarkersGeneral Pathology
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TRPA1 channel is a cardiac target of mIGF-1/SIRT1 signaling.

2014

Cardiac overexpression of locally acting muscle-restricted (m)IGF-1 and the consequent downstream activation of NAD+-dependent protein deacetylase sirtuin 1 (SIRT1) trigger potent cardiac antioxidative and antihypertrophic effects. Transient receptor potential (TRP) cation channel A1 (TRPA1) belongs to the TRP ion channel family of molecular detectors of thermal and chemical stimuli that activate sensory neurons to produce pain. Recently, it has been shown that TRPA1 activity influences blood pressure, but the significance of TRPA1 in the cardiovascular system remains elusive. In the present work, using genomic screening in mouse hearts, we found that TRPA1 is a target of mIGF-1/SIRT1 sign…

Member 1PhysiologyTransgeneHeart; Insulin-like growth factor-1; Member 1; Sirtuin 1; Subfamily A; Transient receptor potential cation channelBlood PressurePharmacologymedicine.disease_causeTransient receptor potential channelMiceTransient Receptor Potential ChannelsSirtuin 1Physiology (medical)medicineAnimalsMyocytes CardiacInsulin-Like Growth Factor IPromoter Regions GeneticTRPA1 Cation ChannelbiologySirtuin 1AntagonistIGF-1 SIRT1 TRPA1 micefood and beveragesHeartTransient receptor potential cation channelInsulin-like growth factor-1Subfamily APurinesbiology.proteinProtein deacetylaseAcetanilidesNAD+ kinaseSignal transductionCardiology and Cardiovascular Medicinepsychological phenomena and processesOxidative stressSignal Transduction
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Genetic ablation of macrohistone H2A1 leads to increased leanness, glucose tolerance and energy expenditure in mice fed a high-fat diet.

2015

Contains fulltext : 155347.pdf (Publisher’s version ) (Closed access) BACKGROUND/OBJECTIVES: In the context of obesity, epigenetic mechanisms regulate cell-specific chromatin plasticity, perpetuating gene expression responses to nutrient excess. MacroH2A1, a variant of histone H2A, emerged as a key chromatin regulator sensing small nutrients during cell proliferation and differentiation. Mice genetically ablated for macroH2A1 (knockout (KO)) do not show overt phenotypes under a standard diet. Our objective was to analyse the in vivo role of macroH2A1 in response to nutritional excess. METHODS: Twelve-week-old whole-body macroH2A1 KO male mice were given a high-fat diet (60% energy from lard…

EXPRESSIONCHROMATINNonalcoholic steatohepatitisModels Molecularmedicine.medical_specialtyHISTONE VARIANT MACROH2Amacrohistone H2A1 High fat diet obesity.Endocrinology Diabetes and MetabolismLIVER-DISEASE NAFLDTHERMOGENESISMedicine (miscellaneous)Adipose tissueBiologyDiet High-FatCell LineHistonesMiceINFLAMMATIONAdipose Tissue BrownThinnessInternal medicineBINDINGmedicineAnimalsGenetic ablationNutrition and DieteticsAdipogenesisNONALCOHOLIC STEATOHEPATITISTRANSCRIPTIONAL COREGULATOR PELP1medicine.diseaseNUTRITION&DIETETICSObesityDisease Models AnimalRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]EndocrinologyEnergy expenditureFat dietOBESITYInsulin ResistanceEnergy MetabolismThermogenesisInternational journal of obesity (2005)
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

2021

Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to…

0301 basic medicineProgrammed cell deathSettore BIO/06AutophagosomeAutolysosome[SDV]Life Sciences [q-bio]lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Autophagy-Related ProteinsReviewComputational biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologySettore MED/0403 medical and health sciencesstressChaperone-mediated autophagyddc:570AutophagyLC3AnimalsHumanscancerSettore BIO/10Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSet (psychology)Molecular Biologyvacuole.phagophore030102 biochemistry & molecular biologyvacuolebusiness.industryInterpretation (philosophy)AutophagyAutophagosomesneurodegenerationCell BiologyfluxMulticellular organismmacroautophagy030104 developmental biologyKnowledge baselysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleBiological AssayLysosomesbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Autophagy

2021

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide…

macroautophagy;autophagyAutophagosome[SDV]Life Sciences [q-bio]canceLC3 macroautophagyautophagosomeneurodegeneration;[SDV.BC]Life Sciences [q-bio]/Cellular BiologyAutophagy AutophagosomeNOstress vacuolestressautophagic processesstrerfluxLC3cancerguidelinesAutophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/06 - Anatomia Comparata E Citologia[SDV.BC] Life Sciences [q-bio]/Cellular BiologyComputingMilieux_MISCELLANEOUSMedaka oryzias latipesphagophorevacuoleQHneurodegenerationAutophagosome cancer flux LC3 lysosome macroautophagy neurodegeneration phagophore stress vacuoleautophagy; autophagic processes; guidelines; autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuolefluxmacroautophagystress.lysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/17 - ISTOLOGIARC
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