Search results for "Inducible"

showing 10 items of 111 documents

Activation and selective IL-17 response of human Vγ9Vδ2 T lymphocytes by TLR-activated plasmacytoid dendritic cells.

2016

// Elena Lo Presti 1,2 , Nadia Caccamo 1,2 , Valentina Orlando 1,2 , Francesco Dieli 1,2 and Serena Meraviglia 1,2 1 Central Laboratory of Advanced Diagnosis and Biomedical Research (CLADIBIOR), University of Palermo, Palermo, Italy 2 Department of Biopathology and Medical Biotechnologies (DIBIMED), University of Palermo, Palermo, Italy Correspondence to: Serena Meraviglia, email: // Keywords : γδ T cells, plasmacytoid dendritic cells, IL-17, TLR activation, proliferation, Immunology and Microbiology Section, Immune response, Immunity Received : July 20, 2016 Accepted : August 02, 2016 Published :August 31, 2016 Abstract Vγ9Vδ2 T cells and plasmacytoid dendritic cells (pDCs) are two distinc…

0301 basic medicineTLR activationCellCell CommunicationLigandsLymphocyte Activation0302 clinical medicineT-Lymphocyte SubsetsCoculture TechniqueAntigen PresentationInterleukin-17Research Paper: Immunologyhemic and immune systemsIL-17medicine.anatomical_structurePhenotypeOncologyplasmacytoid dendritic cellsImmunology and Microbiology SectionInterleukin 17HumanCell typeproliferationCD40 LigandLigandBiologyDendritic Cellγδ T cells03 medical and health sciencesInducible T-Cell Co-Stimulator LigandInterferon-gammaImmune systemImmunityplasmacytoid dendritic cellmedicineHumansImmune responseCell Proliferationγδ T cellCD40Innate immune systemImmunityTLR9Dendritic CellsReceptors OX40Coculture TechniquesImmunity Innate030104 developmental biologyImmunologybiology.proteinLeukocytes MononuclearCpG IslandsCpG IslandImmunologic Memory030215 immunologyOncotarget
researchProduct

Lack of Hypoxic Response in Uterine Leiomyomas despite Severe Tissue Hypoxia

2008

Abstract Hypoxia is now established as a key factor influencing the pathophysiology of malignant growth. Among other effects, hypoxia modulates the expression of a multitude of genes through the induction of hypoxia-inducible transcription factors. This differential gene expression favors angiogenesis, cell survival, an invasive/metastatic phenotype, and resistance to anticancer therapies. Because benign tumors do not exhibit these traits, one might expect these entities to be neither hypoxic nor to induce the genetic hypoxia response program. To test this hypothesis, an investigation of the oxygenation status of 17 leiomyomas and 1 leiomyosarcoma of the uterus using polarographic needle el…

AdultLeiomyosarcomaLeiomyosarcomaCancer ResearchPathologymedicine.medical_specialtyAngiogenesisUterusUterine Cervical NeoplasmsApoptosisBiologyImmunoenzyme TechniquesAntigens NeoplasmBiopsyBasic Helix-Loop-Helix Transcription FactorsIn Situ Nick-End LabelingmedicineHumansProspective StudiesCarbonic Anhydrase IXHypoxiaCarbonic AnhydrasesCell ProliferationGlucose Transporter Type 1Uterine leiomyomaLeiomyomamedicine.diagnostic_testMiddle AgedHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subunitmedicine.diseasePhenotypeOxygenmedicine.anatomical_structureLeiomyomaOncologyMyometriumFemalemedicine.symptomCancer Research
researchProduct

Limb Ischemic Conditioning Induces Oxidative Stress Followed by a Correlated Increase of HIF-1α in Healthy Volunteers.

2019

Background Local and remote ischemic preconditioning has been used as a protective intervention against ischemia/reperfusion (I/R) damage in several preclinical and clinical studies. However, its physiological mechanisms are not completely known. I/R increases the production of reactive oxygen species, which also serve as messengers for a variety of functions. Hypoxia-inducible factor 1 alpha (HIF-1α) is probably the most important transcription factor mediator of hypoxic signaling. Objective We hypothesized that limb ischemic conditioning (LIC) induces a local oxidative/nitrosative stress and a correlated increase of HIF-1α plasma levels. Methods An observational, prospective, and single-c…

AdultMalemedicine.medical_specialtyTime FactorsIschemiaOxidative phosphorylation030204 cardiovascular system & hematologymedicine.disease_causeDinoprost030218 nuclear medicine & medical imagingUpper Extremity03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicineBlood plasmamedicineHumansProspective StudiesNitriteIschemic PreconditioningNitriteschemistry.chemical_classificationReactive oxygen speciesbusiness.industryGeneral MedicineVenous bloodmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitHealthy VolunteersUp-RegulationOxidative StressEndocrinologychemistryNitrosative StressRegional Blood FlowSpainIschemic preconditioningSurgeryFemaleTherapeutic OcclusionCardiology and Cardiovascular MedicinebusinessOxidative stressBiomarkersAnnals of vascular surgery
researchProduct

The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
researchProduct

Novel anti-inflammatory chalcone derivatives inhibit the induction of nitric oxide synthase and cyclooxygenase-2 in mouse peritoneal macrophages

1999

AbstractIn a previous work, we tested a series of chalcone derivatives as possible anti-inflammatory compounds. We now investigate the effects of three of those compounds, CH1, CH8 and CH12, on nitric oxide and prostanoid generation in mouse peritoneal macrophages stimulated with lipopolysaccharide and in the mouse air pouch injected with zymosan, where they showed a dose-dependent inhibition with inhibitory concentration 50% values in the μM range. This effect was not the consequence of a direct inhibitory action on enzyme activities. Our results demonstrated that chalcone derivatives inhibited de novo inducible nitric oxide synthase and cyclooxygenase-2 synthesis, being a novel therapeuti…

LipopolysaccharidesChalconeLipopolysaccharidemedicine.drug_classBiophysicsNitric Oxide Synthase Type IILipopolysaccharidePharmacologyBiochemistryDinoprostoneAnti-inflammatoryNitric oxideMicechemistry.chemical_compoundChalconeStructural BiologyGeneticsmedicineAnimalsCyclooxygenase-2Mouse air pouchInducible nitric oxide synthaseMolecular BiologyNitritesDose-Response Relationship DrugbiologyAnti-Inflammatory Agents Non-SteroidalZymosanZymosanProstanoidMouse peritoneal macrophageCell BiologyIsoenzymesNitric oxide synthasechemistryBiochemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme InductionMacrophages Peritonealbiology.proteinFemaleCyclooxygenaseNitric Oxide SynthaseFEBS Letters
researchProduct

Respiratory plasticity in response to changes in oxygen supply and demand

2011

Aerobic organisms maintain O(2) homeostasis by responding to changes in O(2) supply and demand in both short and long time domains. In this review, we introduce several specific examples of respiratory plasticity induced by chronic changes in O(2) supply (environmental hypoxia or hyperoxia) and demand (exercise-induced and temperature-induced changes in aerobic metabolism). These studies reveal that plasticity occurs throughout the respiratory system, including modifications to the gas exchanger, respiratory pigments, respiratory muscles, and the neural control systems responsible for ventilating the gas exchanger. While some of these responses appear appropriate (e.g., increases in lung su…

Hyperoxia0303 health sciencesOxygen supplyCellular respirationPlant SciencePlasticityBiologyLung surface03 medical and health sciences0302 clinical medicineHypoxia-inducible factorsImmunologymedicineAnimal Science and Zoologymedicine.symptomRespiratory systemNeuroscience030217 neurology & neurosurgeryHomeostasis030304 developmental biologyIntegrative and Comparative Biology
researchProduct

Hypoxia and Aggressive Tumor Phenotype: Implications for Therapy and Prognosis

2008

Abstract Tumor hypoxia, mostly resulting from poor perfusion and anemia, is one of the key factors in inducing the development of cell clones with an aggressive and treatment-resistant phenotype that leads to rapid progression and poor prognosis. Studies in patients with solid tumors suggest that there is a range of hemoglobin (Hb) concentrations that is optimum for tumor oxygenation. When used to achieve an Hb level within this range, erythropoiesis-stimulating agents (ESAs) can be expected to increase tumor oxygenation, and this may favorably influence sensitivity to treatment as well as quality of life. There is no robust evidence that ESAs, when used as indicated, have a negative effect…

OncologyCancer Researchmedicine.medical_specialtyPathologyAnemiaCellHemoglobinsNeoplasmsInternal medicinemedicineHumansErythropoietinCell ProliferationTumor hypoxiabusiness.industryAnemiaCell DifferentiationHypoxia (medical)Tumor OxygenationHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseasePhenotypeCell HypoxiaRecombinant ProteinsOxygenCell Transformation Neoplasticmedicine.anatomical_structureOncologyHematinicsHemoglobinmedicine.symptombusinessPerfusionThe Oncologist
researchProduct

Mutant p53 induces Golgi tubulo-vesiculation driving a prometastatic secretome

2020

TP53 missense mutations leading to the expression of mutant p53 oncoproteins are frequent driver events during tumorigenesis. p53 mutants promote tumor growth, metastasis and chemoresistance by affecting fundamental cellular pathways and functions. Here, we demonstrate that p53 mutants modify structure and function of the Golgi apparatus, culminating in the increased release of a pro-malignant secretome by tumor cells and primary fibroblasts from patients with Li-Fraumeni cancer predisposition syndrome. Mechanistically, interacting with the hypoxia responsive factor HIF1α, mutant p53 induces the expression of miR-30d, which in turn causes tubulo-vesiculation of the Golgi apparatus, leading …

0301 basic medicineBiopsyGeneral Physics and AstronomyGolgi ApparatusAnimals Biopsy Breast Neoplasms Cell Line Tumor Cell Transformation Neoplastic Female Fibroblasts Gene Expression Regulation Neoplastic Golgi Apparatus Humans Hypoxia-Inducible Factor 1 alpha Subunit Li-Fraumeni Syndrome Mice MicroRNAs Microtubules Mutation Primary Cell Culture Secretory Vesicles Signal TransductionSkin Tumor Microenvironment Tumor Suppressor Protein p53 Xenograft Model Antitumor Assays02 engineering and technologymedicine.disease_causeCell TransformationMicrotubulesSettore BIO/09 - FisiologiaMetastasisLi-Fraumeni SyndromeMiceTumor MicroenvironmentGolgisecretory machinerySuper-resolution microscopyAnimals; Biopsy; Breast Neoplasms; Cell Line Tumor; Cell Transformation Neoplastic; Female; Fibroblasts; Gene Expression Regulation Neoplastic; Golgi Apparatus; Humans; Hypoxia-Inducible Factor 1 alpha Subunit; Li-Fraumeni Syndrome; Mice; MicroRNAs; Microtubules; Mutation; Primary Cell Culture; Secretory Vesicles; Signal Transduction; Skin; Tumor Microenvironment; Tumor Suppressor Protein p53; Xenograft Model Antitumor Assayslcsh:ScienceSkinMultidisciplinaryTumorChemistrymutant p53QCell migrationMicroRNASecretomics021001 nanoscience & nanotechnologyCell biologyGene Expression Regulation NeoplasticCell Transformation NeoplasticsymbolsFibroblastmiR-30dFemaleHypoxia-Inducible Factor 10210 nano-technologyBreast NeoplasmHumanSignal TransductionCancer microenvironmentStromal cellSecretory VesicleSciencePrimary Cell CultureBreast NeoplasmsMicrotubuleGolgi ApparatuSettore MED/08 - Anatomia Patologicaalpha SubunitGeneral Biochemistry Genetics and Molecular BiologyArticleCell Line03 medical and health sciencessymbols.namesakeCell Line TumormedicineAnimalsHumansSettore MED/05 - Patologia ClinicaSecretionTumor microenvironmentNeoplasticAnimalSecretory VesiclesGeneral ChemistryOncogenesGolgi apparatusHDAC6FibroblastsMicroreviewHypoxia-Inducible Factor 1 alpha SubunitmicroenvironmentXenograft Model Antitumor AssaysMicroRNAs030104 developmental biologyGene Expression RegulationMutationlcsh:QTumor Suppressor Protein p53Carcinogenesis
researchProduct

Direct conversion of human fibroblast to hepatocytes using a single inducible polycistronic vector

2019

Abstract Background Human fibroblasts can be reprogrammed into induced hepatocyte-like cells through the expression of a set of transcription factors. Although the generation of induced hepatocyte-like cells by HNF4A, HNF1A, and FOXA3 expression has proven to be a robust experimental strategy, using multiple lentivirus results in a highly variable heterogeneous population. Methods We designed and implemented a novel approach based on the delivery of reprogramming factors and green fluorescent protein in a single doxycycline-inducible lentiviral vector using 2A self-cleaving peptides. Results Fibroblasts infected with the lentiviral vector can be amplified in basic fibroblast culture media i…

Male0301 basic medicineInducibleGenetic VectorsGreen Fluorescent ProteinsMedicine (miscellaneous)Biochemistry Genetics and Molecular Biology (miscellaneous)Cell LineViral vectorGreen fluorescent proteinlcsh:BiochemistryMice03 medical and health sciences0302 clinical medicinePolycistronic vectorsmedicineAnimalsHumanslcsh:QD415-436TransgenesFibroblastGeneTranscription factorlcsh:R5-920ChemistryResearchReprogrammingDermisCell BiologyFibroblastsCellular ReprogrammingCell biologyInduced hepatocyte-like cellsiHEPPhenotype030104 developmental biologymedicine.anatomical_structureGenes030220 oncology & carcinogenesisDoxycyclineHepatocytesMolecular MedicineFOXA3Stem celllcsh:Medicine (General)ReprogrammingStem Cell Research & Therapy
researchProduct

Metabolic adaptation and neuroprotection differ in the retina and choroid in a piglet model of acute postnatal hypoxia.

2013

Hypoxic-ischemic insults to the neonatal brain may cause neurodevelopmental disorders. Vulnerability of different areas of the neural tissue to hypoxic-ischemic stress might be explained by either heterogeneous sensitivity to oxygen or neuroprotective capability. Our understanding of regional heterogeneity is still incomplete in terms of metabolic reconfiguration and/or activation of neuroprotective mechanisms.We studied, by western blotting, reverse-transcriptase PCR, and tandem mass spectrometry, the response of retina and choroid at protein, gene, and metabolic levels during hypoxia in a piglet model of acute postnatal hypoxia.We evidenced a metabolic shift towards glycolysis in choroid …

medicine.medical_specialtySwineanimal diseasesBlotting WesternMetabolic adaptationNeuroprotectionRetinafluids and secretionsStress PhysiologicalTandem Mass SpectrometryInternal medicinemedicineAnimalsHypoxiaRetinaintegumentary systembusiness.industryChoroidReverse Transcriptase Polymerase Chain ReactionHypoxia (medical)Hypoxia-Inducible Factor 1 alpha Subuniteye diseasesBlotmedicine.anatomical_structureEndocrinologyAnimals NewbornAnesthesiaPediatrics Perinatology and Child Healthsense organsChoroidmedicine.symptombusinessEnergy MetabolismGlycolysisSignal TransductionPediatric research
researchProduct