0000000000328817

AUTHOR

Jude A. Oben

showing 8 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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Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin.

2021

Abstract Background Nonalcoholic fatty liver disease (NAFLD) is increasingly prevalent and represents a growing challenge in terms of prevention and treatment. A minority of affected patients develops inflammation, subsequently fibrosis, cirrhosis and hepatocellular carcinoma (HCC). HCC is a leading cause of cancer-related death. An increased number of senescent cells correlate with age-related tissue degeneration during NAFLD-induced HCC. Senolytics are promising agents that target selectively senescent cells. Previous studies showed that whereas a combination of the senolytic drugs dasatinib and quercetin (D + Q) reduced NAFLD in mice, D + Q lacked efficacy in removing doxorubicin-induced…

0301 basic medicineMaleAgingCirrhosisDasatiniblcsh:MedicineBiochemistrySenolytics.Liver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseSenotherapeuticsNonalcoholic fatty liver diseaseDiethylnitrosamineCancerlcsh:CytologyLiver Diseases3. Good healthDasatinib030220 oncology & carcinogenesisHepatocellular carcinomaDisease ProgressionQuercetinmedicine.symptomLiver diseasemedicine.drugShort ReportInflammationDiet High-Fat03 medical and health sciencesmedicineAnimalsObesitylcsh:QH573-671SenolyticMolecular BiologyInflammationbusiness.industrySenolyticslcsh:RCell Biologymedicine.diseasedigestive system diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologyGene Expression RegulationCancer researchbusinessCell communication and signaling : CCS
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GDF11 induces mild hepatic fibrosis independent of metabolic health

2020

BACKGROUND & AIMS: Growth Differentiation Factor 11 (GDF11) is an anti-aging factor, yet its role in liver diseases is not established. We evaluated the role of GDF11 in healthy conditions and in the transition from non-alcoholic fatty liver disease (NAFLD) to non-alcoholic steatohepatitis (NASH). RESULTS: GDF11 mRNA levels positively correlated with NAFLD activity score and with CPT1, SREBP, PPAR? and Col1A1 mRNA levels, and associated to portal fibrosis, in morbidly obese patients with NAFLD/NASH. GDF11-treated mice showed mildly exacerbated hepatic collagen deposition, accompanied by weight loss and without changes in liver steatosis or inflammation. GDF11 triggered ALK5-dependent SMAD2/…

Liver CirrhosisMaleAgingSettore MED/09 - Medicina Interna*liverLiver Cirrhosis ExperimentalFetgeWeight lossFibrosisfibrosis; growth differentiation factor 11; liver; NAFLD; NASHNon-alcoholic Fatty Liver DiseaseGrowth differentiation factor 11Fatty liverNASH*fibrosisMiddle AgedObesity MorbidGrowth Differentiation FactorsLiverBone Morphogenetic ProteinsDisease ProgressionFemalemedicine.symptomResearch PaperSignal TransductionAdultmedicine.medical_specialtygrowth differentiation factor 11Inflammationliverdigestive systemCell LineEnvellimentInternal medicineNAFLDmedicineHepatic Stellate CellsAnimalsHumansddc:612*growth differentiation factor 11business.industry*NAFLDfibrosisnutritional and metabolic diseasesCell Biologyliver NAFLD NASH fibrosis growth differentiation factor 11*NASHmedicine.diseaseFibrosisdigestive system diseasesMice Inbred C57BLEndocrinologyPortal fibrosisCase-Control StudiesGDF11Hepatic stellate cellSteatohepatitisHepatic fibrosisbusiness
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Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

2021

Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

endocrine systemhemic and lymphatic diseasesheterocyclic compounds3. Good health
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Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

2021

Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

endocrine systemhemic and lymphatic diseasesheterocyclic compounds3. Good health
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Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

2021

Additional file of Mild exacerbation of obesity- and age-dependent liver disease progression by senolytic cocktail dasatinib + quercetin

Physiology39999 Chemical Sciences not elsewhere classifiedFOS: Chemical sciencesFOS: Biological sciencesFOS: Clinical medicineImmunologyGeneticsBiochemistry69999 Biological Sciences not elsewhere classifiedBiotechnologyCancer
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