Search results for "EPA"

showing 10 items of 8995 documents

Dysregulation of DNA methylation induced by past arsenic treatment causes persistent genomic instability in mammalian cells

2015

The mechanisms by which arsenic-induced genomic instability is initiated and maintained are poorly understood. To investigate potential epigenetic mechanisms, in this study we evaluated global DNA methylation levels in V79 cells and human HaCaT keratinocytes at several time points during expanded growth of cell cultures following removal of arsenite exposures. We have found altered genomic methylation patterns that persisted up to 40 cell generations in HaCaT cells after the treatments were withdrawn. Moreover, mRNA expression levels were evaluated by RT-PCR for DNMT1, DNMT3A, DNMT3B, HMLH1, and HMSH2 genes, demonstrating that the down regulation of DNMT3A and DNMT3B genes, but not DNMT1, o…

0301 basic medicineGenome instabilityEpidemiologyHealth Toxicology and MutagenesisMethylationEpigenomeBiology03 medical and health sciences030104 developmental biologyDNA methylationCancer researchDNA mismatch repairEpigeneticsReprogrammingGenetics (clinical)DNA hypomethylationEnvironmental and Molecular Mutagenesis
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Inhibition of DNA damage response at telomeres improves the detrimental phenotypes of Hutchinson–Gilford Progeria Syndrome

2019

Hutchinson–Gilford progeria syndrome (HGPS) is a genetic disorder characterized by premature aging features. Cells from HGPS patients express progerin, a truncated form of Lamin A, which perturbs cellular homeostasis leading to nuclear shape alterations, genome instability, heterochromatin loss, telomere dysfunction and premature entry into cellular senescence. Recently, we reported that telomere dysfunction induces the transcription of telomeric non-coding RNAs (tncRNAs) which control the DNA damage response (DDR) at dysfunctional telomeres. Here we show that progerin-induced telomere dysfunction induces the transcription of tncRNAs. Their functional inhibition by sequence-specific telomer…

0301 basic medicineGenome instabilityRNA UntranslatedDNA RepairGeneral Physics and AstronomyCellular homeostasisAntisense oligonucleotide therapyMice0302 clinical medicineProgeriaHomeostasislcsh:ScienceCellular SenescenceSkinProgeriaMultidisciplinaryintegumentary systemQTelomereProgerinLamin Type A3. Good healthCell biologyTelomeresPhenotypePremature agingcongenital hereditary and neonatal diseases and abnormalitiesDNA repairScienceDouble-strand DNA breaksBiologySettore MED/08 - Anatomia PatologicaGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencesmedicineDNA damage Hutchinson-Gilford Progeria SyndromeAnimalsCell Proliferationnutritional and metabolic diseasesGeneral ChemistryOligonucleotides Antisensemedicine.diseaseTelomereDisease Models Animal030104 developmental biologyMutationlcsh:Q030217 neurology & neurosurgeryLaminDNA DamageNature Communications
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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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Exome-Wide Association Study on Alanine Aminotransferase Identifies Sequence Variants in the GPAM and APOE Associated With Fatty Liver Disease.

2021

BACKGROUND & AIMS: Fatty liver disease (FLD) is a growing epidemic that is expected to be the leading cause of end-stage liver disease within the next decade. Both environmental and genetic factors contribute to the susceptibility of FLD. Several genetic variants contributing to FLD have been identified in exome-wide association studies. However, there is still a missing hereditability indicating that other genetic variants are yet to be discovered. METHODS: To find genes involved in FLD, we first examined the association of missense and nonsense variants with alanine amino transferase at an exome-wide level in 425,671 participants from the UK Biobank. We then validated genetic variants wit…

0301 basic medicineGenome-wide association studyLiver disease0302 clinical medicineENRICHMENT ANALYSISNon-alcoholic Fatty Liver DiseaseRisk FactorsNonalcoholic fatty liver diseaseExomeCONFERS SUSCEPTIBILITYGeneticsINSULIN-RESISTANCEmedicine.diagnostic_testFatty liverGastroenterologyAlanine Transaminase1-Acylglycerol-3-Phosphate O-Acyltransferase3. Good healthGENOMEEuropePhenotypeLiver biopsy030211 gastroenterology & hepatologyNonalcoholic Fatty Liver DiseaseMAFLDSingle-nucleotide polymorphismBiologyTransaminaseRisk Assessment03 medical and health sciencesApolipoproteins ENAFLDmedicineGenetic predispositionHumansGenetic Predisposition to DiseaseHEPATIC STEATOSISGenetic associationMAFLD Phenotype Reproducibility of Results Risk Assessment Risk Factors Transcriptome Genetic Variation Metabolic Associated Fatty Liver Disease Nonalcoholic Fatty Liver Disease Transaminase 1-Acylglycerol-3-Phosphate O-Acyltransferase Alanine Transaminase Apolipoproteins E Biomarkers Europe Exome Gene Expression Profiling Genetic Predisposition to Disease Genome-Wide Association Study Humans Non-alcoholic Fatty Liver DiseaseHepatologyMUTATIONSGene Expression ProfilingGenetic VariationReproducibility of Resultsmedicine.diseaseX-RECEPTORGENE030104 developmental biology3121 General medicine internal medicine and other clinical medicineMetabolic Associated Fatty Liver DiseaseRNA-SEQ DATATranscriptomePATHOGENICITYBiomarkersGenome-Wide Association StudyGastroenterology
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IFNL3/4 genotype is associated with altered immune cell populations in peripheral blood in chronic hepatitis C infection

2016

Single-nucleotide polymorphisms near the interferon lambda 3 (IFNL3) gene predict outcomes to infection and anti-viral treatment in hepatitis C virus (HCV) infection. To identify IFNL3 genotype effects on peripheral blood, we collected phenotype data on 400 patients with genotype 1 chronic hepatitis C (CHC). The IFNL3 responder genotype predicted significantly lower white blood cells (WBCs), as well as lower absolute numbers of monocytes, neutrophils and lymphocytes for both rs8099917 and rs12979860. We sought to define the WBC subsets driving this association using flow cytometry of 67 untreated CHC individuals. Genotype-associated differences were seen in the ratio of CD4CD45RO+ to CD4CD4…

0301 basic medicineGenotypeTranscription FactorT-LymphocytesHepatitis C virusImmunologyHepacivirusBiologymedicine.disease_causeMonocyteMonocytesCohort Studies03 medical and health sciencesGeneticInterferonGenotypeGeneticsmedicineHumansGenetics (clinical)Whole bloodHepaciviruInterleukinsMonocyteGATA3Hepatitis CHepatitis C ChronicInterleukinViral Loadmedicine.diseaseFlow CytometryAntigens Differentiation3. Good healthKiller Cells Natural030104 developmental biologymedicine.anatomical_structureT-LymphocyteImmunologyOriginal ArticleInterferonsCohort StudieViral loadTranscription Factorsmedicine.drugHuman
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Viral resistance in HCV infection.

2018

The introduction of new multi-genotypic direct acting antivirals (DAA) in clinical practice has revolutionized HCV treatment, permitting the achievement of >95% rates of sustained virological response in many patients. However, virological failures can occur particularly if the treatments are sub optimal and/or with too short duration. Failure is often associated with development of resistance. The wide genetic variability in terms of different genotypes and subtypes, together with the natural presence and/or easy development of resistance during treatment, are intrinsic characteristics of HCV that may affect the treatment outcome and the chances of achieving a virological cure. This review…

0301 basic medicineGenotypeTreatment outcomeDrug ResistanceDrug resistanceHepacivirusBiologyViral resistanceAntiviral AgentsVirological response03 medical and health sciences0302 clinical medicinePharmacotherapyDrug TherapyDrug Resistance Multiple ViralVirologyRibavirinmedicineHumansGenetic variabilityViralTreatment FailureChronicAntiviral Agents; Drug Therapy Combination; Genetic Variation; Genotype; Hepacivirus; Hepatitis C Chronic; Humans; Interferons; Ribavirin; Treatment Failure; Drug Resistance Multiple ViralGenetic VariationHepatitis CHepatitis C Chronicmedicine.diseaseSettore MED/07 - Microbiologia e Microbiologia ClinicaHepatitis C030104 developmental biologyHCVImmunologyCombinationHcv treatment030211 gastroenterology & hepatologyDrug Therapy CombinationInterferonsMultipleCurrent opinion in virology
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Duodenal Bacteria From Patients With Celiac Disease and Healthy Subjects Distinctly Affect Gluten Breakdown and Immunogenicity

2016

Background & Aims Partially degraded gluten peptides from cereals trigger celiac disease (CD), an autoimmune enteropathy occurring in genetically susceptible persons. Susceptibility genes are necessary but not sufficient to induce CD, and additional environmental factors related to unfavorable alterations in the microbiota have been proposed. We investigated gluten metabolism by opportunistic pathogens and commensal duodenal bacteria and characterized the capacity of the produced peptides to activate gluten-specific T-cells from CD patients. Methods We colonized germ-free C57BL/6 mice with bacteria isolated from the small intestine of CD patients or healthy controls, selected for their in v…

0301 basic medicineGlutensDuodenumTissue transglutaminaseT-Lymphocytesdigestive systemMicrobiologyMice03 medical and health sciencesLactobacillusmedicineAnimalsHumansImmunogenetic Phenomenachemistry.chemical_classificationHepatologybiologyImmunogenicityGastroenterologynutritional and metabolic diseasesmedicine.diseasebiology.organism_classificationGlutendigestive system diseasesSmall intestineAltered Schaedler floraMice Inbred C57BLCeliac DiseaseLactobacillus030104 developmental biologymedicine.anatomical_structurechemistryBacterial TranslocationCase-Control StudiesPseudomonas aeruginosaImmunologybiology.proteinGliadinDysbiosisGastroenterology
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Adipocytes as a Link Between Gut Microbiota-Derived Flagellin and Hepatocyte Fat Accumulation

2016

While the role of both elevated levels of circulating bacterial cell wall components and adipose tissue in hepatic fat accumulation has been recognized, it has not been considered that the bacterial components-recognizing adipose tissue receptors contribute to the hepatic fat content. In this study we found that the expression of adipose tissue bacterial flagellin (FLG)-recognizing Toll-like receptor (TLR) 5 associated with liver fat content (r = 0.699, p = 0.003) and insulin sensitivity (r = -0.529, p = 0.016) in humans (n = 23). No such associations were found for lipopolysaccharides (LPS)-recognizing TLR4. To study the underlying molecular mechanisms of these associations, human HepG2 he…

0301 basic medicineGlycerollcsh:MedicineAdipose tissueWhite adipose tissueflagellinBiochemistryImmune ReceptorsFatsEndocrinologyAnimal CellsAdipocytesMedicine and Health SciencesInsulinlcsh:ScienceToll-like ReceptorsConnective Tissue CellsMultidisciplinaryImmune System ProteinsbiologyLiver DiseasesFatty liverin kaltaiset reseptorit [toll]Lipidsadipose tissuePhysical sciencesChemistryMitochondrial respiratory chainAdipose TissueConnective Tissuebacterial componentsCellular TypesAnatomyinsuline sensitivityResearch ArticleSignal Transductionmedicine.medical_specialtyadipocytesImmunologyMonomers (Chemistry)Gastroenterology and Hepatologyta311103 medical and health sciencesInsulin resistanceInternal medicinemedicinePolymer chemistryDiabetic Endocrinologylcsh:Rta1183ta1182Biology and Life SciencesProteinsCell Biologyliver fatmedicine.diseasehepatic fatfat accumulationHormonesIRS1Fatty LiverInsulin receptor030104 developmental biologyEndocrinologyBiological TissueTLR5biology.proteinlcsh:QPLoS ONE
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Efficacy of interleukin 10 gene hydrofection in pig liver vascular isolated ‘in vivo’ by surgical procedure with interest in liver transplantation

2019

AIM Liver transplantation is the only curative strategy for final stage liver diseases. Despite the great advances achieved during the last 20 years, the recipient immune response after transplantation is not entirely controlled. This results in high rates of acute cell rejection and, approximately, 10% of early mortality. Therapeutic treatment could be improved by efficiently transfecting genes that encode natural immunosuppressant proteins, employing safe procedures that could be transferred to clinical setting. In this sense, interleukin 10 plays a central role in immune tolerance response by acting at different levels. METHODS hIL10 gene was hydrofected by retrograde hydrodynamic inject…

0301 basic medicineGraft RejectionCardiovascular ProceduresSwinePhysiologymedicine.medical_treatmentGene TransferVascular SurgeryLiver transplantationPharmacologyImmune tolerance0302 clinical medicineImmune PhysiologyMedicine and Health SciencesMammalsInnate Immune SystemMultidisciplinaryQRGene Transfer TechniquesEukaryotaBlood proteinsRecombinant ProteinsInterleukin-10Interleukin 10LiverVertebratesModels AnimalMedicineCytokines030211 gastroenterology & hepatologyFemaleAnatomyResearch ArticlePlasmidsScienceImmunologyGenetic VectorsSurgical and Invasive Medical ProceduresResearch and Analysis MethodsInjectionsEnd Stage Liver Disease03 medical and health sciencesDigestive System ProceduresGene DeliveryImmune systemIn vivomedicineGene Expression and Vector TechniquesGeneticsImmune ToleranceAnimalsHumansMolecular Biology TechniquesMolecular BiologyTransplantationMolecular Biology Assays and Analysis Techniquesbusiness.industryOrganismsBiology and Life SciencesOrgan TransplantationGenetic TherapyMolecular DevelopmentLiver TransplantationTransplantation030104 developmental biologyImmune SystemAmniotesHydrodynamicsLiver functionbusinessDevelopmental BiologyPLoS ONE
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