Search results for "gene silencing"

showing 10 items of 216 documents

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
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Blocking CD248 molecules in perivascular stromal cells of patients with systemic sclerosis strongly inhibits their differentiation toward myofibrobla…

2018

Abstract Background Fibrosis may be considered the hallmark of systemic sclerosis (SSc), the end stage triggered by different pathological events. Transforming growth factor-β (TGF-β) and platelet-derived growth factor BB (PDGF-BB) are profibrotic molecules modulating myofibroblast differentiation and proliferation, respectively. There is evidence linking CD248 with these two molecules, both highly expressed in patients with SSc, and suggesting that CD248 may be a therapeutic target for several diseases. The aim of this work was to evaluate the expression of CD248 in SSc skin and its ability to modulate SSc fibrotic process. Methods After ethical approval was obtained, skin biopsies were co…

0301 basic medicineMalelcsh:Diseases of the musculoskeletal systemProton Pump InhibitorFibrosiCellular differentiationmedicine.medical_treatmentSystemic sclerosiFibrosisImmunology and AllergyMedicineMyofibroblastsskin and connective tissue diseasesCells CulturedSkinintegumentary systemCell DifferentiationMiddle AgedMesenchymal Stem CellBenzamidesSystemic sclerosisFemaleMyofibroblastResearch ArticleHumanAdultStromal cellImmunology03 medical and health sciencesYoung AdultRheumatologyBenzamideAntigens CDAntigens NeoplasmHumansGene silencingCell ProliferationMyofibroblastScleroderma Systemicbusiness.industryGrowth factorMesenchymal stem cellStromal CellMesenchymal Stem CellsProton Pump Inhibitorsmedicine.diseaseFibrosisCD248Settore MED/16 - Reumatologia030104 developmental biologyCancer researchStromal Cellslcsh:RC925-935CD248; Fibrosis; Systemic sclerosis; Rheumatology; Immunology and Allergy; ImmunologybusinessTransforming growth factor
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MUC1 deficiency mediates corticosteroid resistance in chronic obstructive pulmonary disease.

2018

Background Lung inflammation in COPD is poorly controlled by inhaled corticosteroids (ICS). Strategies to improve ICS efficacy or the search of biomarkers who may select those patients candidates to receive ICS in COPD are needed. Recent data indicate that MUC1 cytoplasmic tail (CT) membrane mucin can mediate corticosteroid efficacy in chronic rhinosinusitis. The objective of this work was to analyze the previously unexplored role of MUC1 on corticosteroid efficacy in COPD in vitro and in vivo models. Methods MUC1-CT expression was measured by real time PCR, western blot, immunohistochemistry and immunofluorescence. The inflammatory mediators IL-8, MMP9, GM-CSF and MIP3α were measured by EL…

0301 basic medicineMalemedicine.drug_classDrug ResistanceInflammationMUC1Corticosteroid resistancedigestive system03 medical and health sciencesMicePulmonary Disease Chronic Obstructive0302 clinical medicineGlucocorticoid receptorIn vivoAdrenal Cortex HormonesmedicineAnimalsHumansGene Silencingskin and connective tissue diseasesneoplasmsDexamethasoneMUC1Agedlcsh:RC705-779Mice KnockoutCOPDLungbusiness.industryResearchChronic obstructive pulmonary diseaseMucin-1Sputumlcsh:Diseases of the respiratory systemMiddle Agedmedicine.diseasedigestive system diseasesrespiratory tract diseasesMice Inbred C57BL030104 developmental biologymedicine.anatomical_structure030228 respiratory systemImmunologyCorticosteroidFemalemedicine.symptombusinessBiomarkersmedicine.drugRespiratory research
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IL-17A-associated IKK-α signaling induced TSLP production in epithelial cells of COPD patients.

2018

Thymic stromal lymphopoietin (TSLP) is a cytokine expressed in the epithelium, involved in the pathogenesis of chronic disease. IL-17A regulates airway inflammation, oxidative stress, and reduction of steroid sensitivity in chronic obstructive pulmonary disease (COPD). TSLP and IL-17A were measured in induced sputum supernatants (ISs) from healthy controls (HC), healthy smokers (HS), and COPD patients by enzyme-linked immunosorbent assay. Human bronchial epithelial cell line (16HBE) and normal bronchial epithelial cells were stimulated with rhIL-17A or ISs from COPD patients to evaluate TSLP protein and mRNA expression. The effects of the depletion of IL-17A in ISs, an anticholinergic drug,…

0301 basic medicineMalemedicine.medical_treatmentClinical Biochemistrylcsh:MedicineCell CountBiochemistryCholinergic AntagonistsPathogenesisHistonesPulmonary Disease Chronic Obstructivelcsh:QD415-436COPDKinaseInterleukin-17AcetylationI-kappa B KinaseRespiratory Function TestsCytokinemedicine.anatomical_structureMolecular MedicineCytokinesFemaleProtein BindingSignal TransductionThymic stromal lymphopoietinEnzyme-Linked Immunosorbent AssayRespiratory MucosaArticleCell Linelcsh:Biochemistry03 medical and health sciencesThymic Stromal LymphopoietinmedicineGene silencingCOPDHumansMolecular Biologybusiness.industrylcsh:RSputumEpithelial Cellsmedicine.diseaseEpitheliumrespiratory tract diseases030104 developmental biologyCell cultureCancer researchbusinessBiomarkersExperimentalmolecular medicine
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Specific role of N-methyl-D-aspartate (NMDA) receptor in elastin-derived VGVAPG peptide-dependent calcium homeostasis in mouse cortical astrocytes in…

2019

AbstractUnder physiological and pathological conditions, elastin is degraded to produce elastin-derived peptides (EDPs). EDPs are detected in the healthy human brain, and its concentration significantly increases after ischemic stroke. Both elastin and EDPs contains replications of the soluble VGVAPG hexapeptide, which has a broad range of biological activities. Effects of VGVAPG action are mainly mediated by elastin-binding protein (EBP), which is alternatively spliced, enzymatically inactive form of the GLB1 gene. This study was conducted to elucidate the activation and role of the N-methyl-D-aspartate receptor (NMDAR) in elastin-derived VGVAPG peptide-dependent calcium homeostasis in mou…

0301 basic medicineMolecular biologylcsh:MedicinePathogenesisBiochemistryReceptors N-Methyl-D-AspartateArticleMice03 medical and health sciencesMedical research0302 clinical medicineAnimalsHomeostasisGene silencingGene SilencingRNA MessengerRNA Small InterferingReceptorlcsh:ScienceCells CulturedCerebral CortexGene knockdownMultidisciplinaryMolecular medicinebiologyChemistrylcsh:RIn vitroElastinCell biology030104 developmental biologyAstrocytesbiology.proteinNMDA receptorCalciumlcsh:QSignal transductionReactive Oxygen SpeciesOligopeptidesElastinBiomarkers030217 neurology & neurosurgeryProto-oncogene tyrosine-protein kinase SrcScientific Reports
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The role of miR-26a and miR-30b in HER2+ breast cancer trastuzumab resistance and regulation of the CCNE2 gene

2016

AbstractA subset of HER2+ breast cancer patients manifest clinical resistance to trastuzumab. Recently, miR-26a and miR-30b have been identified as trastuzumab response regulators, and their target gene CCNE2 seems to play an important role in resistance to trastuzumab therapy. Cell viability was evaluated in trastuzumab treated HER2+ BT474 wt (sensitive), BT474r (acquired resistance), HCC1954 (innate resistance), and MDA-MB-231 (HER2−) cell lines, and the expression of miR-26a, miR-30b, and their target genes was measured. BT474 wt cell viability decreased by 60% and miR-26a and miR-30b were significantly overexpressed (~3-fold, p = 0.003 and p = 0.002, respectively) after trastuzumab trea…

0301 basic medicineOncologyMama -- Càncer -- Aspectes genèticsmedicine.medical_specialtyCell SurvivalReceptor ErbB-2Down-RegulationMama -- Càncer -- TractamentBreast NeoplasmsDrug resistanceArticle03 medical and health sciences0302 clinical medicineBreast cancerTrastuzumabInternal medicineCell Line TumorCyclinsmedicineGene silencingHumansViability assayGene SilencingReceptorskin and connective tissue diseasesneoplasmsRegulation of gene expressionMultidisciplinarybusiness.industryCell CycleTrastuzumabmedicine.diseaseNeoplasm ProteinsGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologyCell cultureDrug Resistance Neoplasm030220 oncology & carcinogenesisFemalebusinessmedicine.drugScientific Reports
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Anticancer properties of 4-thiazolidinone derivatives depend on peroxisome proliferator-activated receptor gamma (PPARγ)

2017

Peroxisome proliferator-activated receptors (PPARs) play an important role in numerous chronic diseases such as diabetes, obesity, atherosclerosis and cancer, and PPAR modulators are among the approved drugs and drug-candidates for their treatment. The aim of this study was to elucidate the involvement of PPARs in the mechanism of cytotoxic and pro-apoptotic action of novel anticancer 4-thiazolidinone derivatives (Les-2194, Les-3377, Les-3640) and approved 4-thiazolidinones (Rosiglitazone, Pioglitazone) towards the human squamous carcinoma (SCC-15) cell line. Experiments with 4-thiazaolidinone derivatives and PPAR-specific siRNA were conducted and PPARα, PPARβ and PPARγ mRNA expression was …

0301 basic medicinePPARsCytotoxicityPeroxisome proliferator-activated receptorAntineoplastic AgentsApoptosisPharmacologySCC-1503 medical and health sciencesStructure-Activity Relationship0302 clinical medicineCell Line TumorDrug DiscoverymedicineGene silencingHumansViability assayRNA MessengerReceptorCell ProliferationPharmacologychemistry.chemical_classificationGene knockdownDose-Response Relationship DrugMolecular StructureThiazolothiopyranesOrganic ChemistryGeneral MedicineSquamous carcinomaPPAR gamma030104 developmental biologychemistryCell cultureThiazolidinone030220 oncology & carcinogenesisThiazolidinesDrug Screening Assays AntitumorRosiglitazonemedicine.drugEuropean Journal of Medicinal Chemistry
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Role of p62/SQSTM1 beyond autophagy: a lesson learned from drug-induced toxicity in vitro

2018

Background and Purpose SQSTM1/p62 is a multifunctional, stress-induced, scaffold protein involved in multiple cellular processes including autophagic clearance, regulation of inflammatory responses and redox homeostasis. Its altered function has been associated with different human pathologies, such as neurodegenerative, metabolic and bone diseases (down-regulation), and cancerogenesis (up-regulation). However, its role in the off-target effects of clinically used drugs is still not understood. Experimental Approach We evaluated the expression of p62 in cultured Hep3B cells and their derived ρ° cells (lacking mitochondria), along with markers of autophagy and mitochondrial dysfunction. The …

0301 basic medicinePharmacologyMitochondrial ROSScaffold proteinAutophagyATG5InflammasomePharmacologyMitochondrionBiologyCell biology03 medical and health sciences030104 developmental biologymedicineGene silencingViability assaymedicine.drugBritish Journal of Pharmacology
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Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.

2018

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

0301 basic medicinePhysiologyCell SurvivalEndogenyApoptosisCell LineSmall hairpin RNA03 medical and health sciences0302 clinical medicinePhysiology (medical)ExtracellularmedicineGene silencingAnimalsMyocytes CardiacGene SilencingGuanine Nucleotide-Releasing Factor 2Cell Proliferationbcl-2-Associated X ProteinPharmacologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Cell growthChemistryHypoxia (medical)PhosphoproteinsCell biologyRats030104 developmental biologyApoptosis030220 oncology & carcinogenesisPhosphorylationmedicine.symptomClinical and experimental pharmacologyphysiology
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Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

2018

Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitising products. A number of studies have shown the presence of TCS in different human tissues such as blood, adipose tissue, the liver, brain as well as in breast milk and urine. N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are widely expressed in the central nervous system and which play key roles in excitatory synaptic transmission. There is, however, no data on the involvement of NMDAR subunits in the apoptotic and neurotoxic effects of TCS. Our experiments are the first to show that TCS used at environmentally relevant concentrations evoked NMDA-dependent effe…

0301 basic medicineProgrammed cell deathGluN1Protein subunitNeurotoxinsNeuroscience (miscellaneous)Glutamic AcidCaspase 3ApoptosisReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsGene SilencingRNA MessengerReceptorNeuronsL-Lactate DehydrogenaseChemistryCaspase 3fungiNeurotoxicityROSTransfectionmedicine.diseaseTriclosanCell biologyGluN2BGluN2AProtein Subunits030104 developmental biologyNeurologyNMDAApoptosisNMDA receptorFemale030217 neurology & neurosurgeryMolecular Neurobiology
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