Search results for "Inducible"

showing 10 items of 111 documents

Elevated protein carbonyl and HIF-1α levels in eyes with proliferative diabetic retinopathy.

2013

Purpose: To evaluate the role of protein carbonyls and hypoxia inducible factor-1a (HIF-1a) in diabetic eyes with proliferative diabetic retinopathy (PDR). Methods: Prospective consecutive controlled observational study was performed. Vitreous samples were collected at the start of the 3-ppp vitrectomy. Protein carbonylation analysis was performed by Western blotting with antibody against 2,4-Dinitrophenol (anti-DNP), following derivatization of protein carbonyls with 2,4 Dinitrophenylhydrazine (DNHP). Protein carbonylation was quantified by scanning densitometry analysis and relativized to the total amount of protein into the ponceau staining of membranes. Vitreous HIF-1 a was determined w…

AdultMaleVascular Endothelial Growth Factor Amedicine.medical_specialtygenetic structuresmedicine.medical_treatmentProtein CarbonylationBlotting WesternVitrectomyEnzyme-Linked Immunosorbent Assaymedicine.disease_causePathogenesisProtein Carbonylationchemistry.chemical_compoundOphthalmologyVitrectomymedicineHumansProspective StudiesMacular holeAgedGlycated HemoglobinDiabetic Retinopathybusiness.industryRetinal detachmentGeneral MedicineDiabetic retinopathyMiddle Agedmedicine.diseaseHypoxia-Inducible Factor 1 alpha Subuniteye diseasesSurgeryVascular endothelial growth factorVitreous BodyOphthalmologyOxidative StressDiabetes Mellitus Type 1chemistryDiabetes Mellitus Type 2Femalesense organsbusinessOxidative stressActa ophthalmologica
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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
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Development and Aging Are Oxygen-Dependent and Correlate with VEGF and NOS along Life Span

2012

During development and aging, vascular remodeling represents a critical adaptive response to modifications in oxygen supply to tissues. Hypoxia inducible factor (HIF) has a crucial role and is modulated by oxygen levels, with an age-dependent response in neonates, adult, and aged people. ROS are generated under hypoxic conditions and the accumulation of free radicals during life reduces the ability of tissues to their removal. In this immunohistochemical study we investigated the presence and localization of VEGF and iNOS in human carotid bodies (CB) sampled at autopsy from three children (mean age – 2 years), four adult young subjects (mean age – 44.3 years), and four old subjects (mean ag…

AdultVascular Endothelial Growth Factor AAgingmedicine.medical_specialtyNitric Oxide Synthase Type IIAutopsyBiologyHypoxemiaNitric oxideYoung Adultchemistry.chemical_compoundAnoxiaInternal medicinemedicineHumansYoung adultChildPreschoolAgedCarotid BodyAdult; Aged; Aging; Anoxia; Carotid Body; Cell Differentiation; Child Preschool; Humans; Nitric Oxide Synthase Type II; Oxygen; Vascular Endothelial Growth Factor A; Young AdultCell DifferentiationHypoxia (medical)Oxygenmedicine.anatomical_structureEndocrinologyHypoxia-inducible factorschemistryImmunohistochemistryCarotid bodymedicine.symptom
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Inducible Co-Stimulator Null MRL-Fas lpr Mice

2005

MRL/MpJ-Tnfrsf6lpr (MRL-Faslpr) mice develop a spontaneous T cell-dependent autoimmune disease that shares features with human lupus, including fatal nephritis, systemic pathology, and autoantibodies (autoAb). The inducible co-stimulator (ICOS) is upregulated on activated T cells and modulates T cell-mediated responses. To investigate whether ICOS has an essential role in regulating autoimmune lupus nephritis and the systemic illness in MRL-Faslpr mice, ICOS null (-/-) MRL Faslpr and ICOS intact (+/+) MRL-Faslpr strains (wild-type [WT]) were generated and compared. It was determined that in ICOS-/- MRL-Faslpr as compared with the WT strain, (1) there is a significant reduction in circulatin…

Antigens Differentiation T-LymphocyteMice Inbred MRL lprT-LymphocytesT cellLupus nephritismedicine.disease_causeBlood Urea NitrogenAutoimmunityInducible T-Cell Co-Stimulator ProteinInterferon-gammaMiceImmune systemimmune system diseasesmedicineAnimalsskin and connective tissue diseasesAutoantibodiesMice Inbred C3HSystemic lupus erythematosusTumor Necrosis Factor-alphabusiness.industryAutoantibodyGeneral Medicinemedicine.diseaseLupus NephritisIsotypeInterleukin-10Mice Inbred C57BLProteinuriamedicine.anatomical_structureNephrologyImmunoglobulin GImmunologyInterleukin-4businessNephritisJournal of the American Society of Nephrology
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The role of ICOS in directing T cell responses: ICOS-dependent induction of T cell anergy by tolerogenic dendritic cells.

2009

Abstract Tolerogenic dendritic cells (DC) play an important role in maintaining peripheral T cell tolerance in steady-state conditions through induction of anergic, IL-10-producing T cells with suppressive properties. ICOS, an activation-induced member of the CD28 family on T cells, is involved in the induction of IL-10, which itself could contribute to induction of anergy and development of suppressive T cells. Therefore, we analyzed the functional role of ICOS in the differentiation process of human CD4+ T cells upon their interaction with tolerogenic DC. We compared the functional properties of CD4+ T cells from healthy volunteers and ICOS-deficient patients after stimulation with tolero…

Antigens Differentiation T-LymphocyteT cellT-LymphocytesImmunologyLymphocyte ActivationT-Lymphocytes RegulatoryInducible T-Cell Co-Stimulator ProteinInterleukin 21medicineImmunology and AllergyCytotoxic T cellHumansIL-2 receptorAntigen-presenting cellCells CulturedClonal AnergyChemistryPeripheral toleranceCell DifferentiationDendritic CellsNatural killer T cellCoculture TechniquesCell biologyInterleukin-10ICOS LIGANDmedicine.anatomical_structureCommon Variable ImmunodeficiencyGene Knockdown TechniquesImmunologyJournal of immunology (Baltimore, Md. : 1950)
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Importance of the inducible costimulator molecule for the induction of allergic immune responses and its decreased expression on T helper cells after…

2004

The inducible costimulator (ICOS), a newly identified member of the CD28 receptor family that is induced after T-cell activation, and its ligand (ICOSL), being expressed on activated monocytes and dendritic cells play a key role in T-cell-mediated immune responses. As ICOS costimulation also seems to regulate T helper 2 effector cells, the aim of this study was to analyse the function of this molecule in allergic immune responses and their specific therapy, mainly venom immunotherapy (VIT). CD4+ T cells from grass pollen-, or bee or wasp venom-allergic donors were stimulated in the presence of autologous mature dendritic cells, which were pulsed with different allergen doses. In this system…

Antigens Differentiation T-Lymphocytemedicine.medical_treatmentImmunologyReceptors Antigen T-CellBiologyLymphocyte ActivationInducible T-Cell Co-Stimulator ProteinTh2 CellsImmune systemAntigenHypersensitivitymedicineHumansImmunology and AllergyInducible T-Cell Co-Stimulator ProteinReceptorArthropod VenomsHistocompatibility Antigens Class IICD28InterleukinOriginal ArticlesDendritic CellsImmunotherapyAllergensTh1 CellsCoculture TechniquesInterleukin-10CytokineDesensitization ImmunologicImmunologyImmunotherapyImmunology
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Multiple in vitro and in vivo regulatory effects of budesonide in CD4+ T lymphocyte subpopulations of allergic asthmatics.

2012

Abstract BACKGROUND: Increased activation and increased survival of T lymphocytes characterise bronchial asthma. OBJECTIVES: In this study the effect of budesonide on T cell survival, on inducible co-stimulator T cells (ICOS), on Foxp3 and on IL-10 molecules in T lymphocyte sub-populations was assessed. METHODS: Cell survival (by annexin V binding) and ICOS in total lymphocytes, in CD4+/CD25+ and in CD4+/CD25- and Foxp3 and IL-10 in CD4+/CD25+ and in CD4+/CD25-cells was evaluated, by cytofluorimetric analysis, in mild intermittent asthmatics (n = 19) and in controls (n = 15). Allergen induced T lymphocyte proliferation and the in vivo effects of budesonide in mild persistent asthmatics (n =…

BudesonideCD4-Positive T-LymphocytesMalePulmonologylcsh:Medicineimmune system diseasesT-Lymphocyte SubsetsMolecular Cell Biologylcsh:ScienceBudesonidecigarette smoke airway epithelial cells reactive oxygen species.MultidisciplinaryT CellsAllergy and HypersensitivityClinical Pharmacologyhemic and immune systemsForkhead Transcription Factorsrespiratory systemMiddle AgedFlow CytometryBronchodilator AgentsInterleukin-10Interleukin 10MedicineFemalemedicine.drugResearch ArticleAdultDrugs and DevicesAdolescentCell SurvivalImmune CellsImmunologychemical and pharmacologic phenomenaInducible T-Cell Co-Stimulator ProteinImmunomodulationIn vivomedicineHumansInducible T-Cell Co-Stimulator ProteinBiologyAsthmaCell Proliferationbusiness.industrylcsh:RT lymphocytemedicine.diseaseIn vitroAsthmarespiratory tract diseasesApoptosisImmunologylcsh:QClinical ImmunologybusinessCytometryPloS one
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Induction of CD36 and thrombospondin-1 in macrophages by hypoxia-inducible factor 1 and its relevance in the inflammatory process.

2012

Inflammation is part of a complex biological response of vascular tissue to pathogens or damaged cells. First inflammatory cells attempt to remove the injurious stimuli and this is followed by a healing process mediated principally by phagocytosis of senescent cells. Hypoxia and p38-MAPK are associated with inflammation, and hypoxia inducible factor 1 (HIF-1) has been detected in inflamed tissues. We aimed to analyse the role of p38-MAPK and HIF-1 in the transcriptional regulation of CD36, a class B scavenger receptor, and its ligand thrombospondin (TSP-1) in macrophages and to evaluate the involvement of this pathway in phagocytosis of apoptotic neutrophils. We have also assessed HIF-1α, p…

CD36 AntigensMaleAnatomy and PhysiologyNeutrophilsCD36Digestive Physiologylcsh:MedicineApoptosisp38 Mitogen-Activated Protein KinasesBiochemistryMonocytesThrombospondin 1Intestinal mucosaCrohn DiseaseIntestinal Mucosalcsh:ScienceHypoxiaPromoter Regions GeneticMultidisciplinaryProtein StabilityMiddle AgedOxygen Metabolismmedicine.anatomical_structureMedicineFemaleHypoxia-Inducible Factor 1medicine.symptomProtein BindingSignal TransductionResearch ArticleAdultCell PhysiologyAdolescentPhagocytosisImmune CellsImmunologyInflammationGastroenterology and HepatologyBiologyCell LineYoung AdultPhagocytosismedicineHumansUlcerative ColitisScavenger receptorBiologyInflammationLamina propriaDigestive RegulationMacrophageslcsh:RInflammatory Bowel DiseaseHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMetabolismApoptosisImmunologyCancer researchbiology.proteinlcsh:QColitis UlcerativeDigestive SystemPloS one
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The role of hypoxia-induced factors in tumor progression.

2004

Abstract Learning Objectives After completing this course, the reader will be able to: Describe hypoxia-induced mechanisms for cell survival. Discuss hypoxia-induced gene expression. Relate hypoxia and glucose metabolism. Access and take the CME test online and receive 1 hour of AMA PRA category 1 credit atCME.TheOncologist.com Hypoxia is a common characteristic of locally advanced solid tumors that has been associated with diminished therapeutic response and, more recently, with malignant progression, that is, an increasing probability of recurrence, locoregional spread, and distant metastasis. Emerging evidence indicates that the effect of hypoxia on malignant progression is mediated by a…

Cancer ResearchAngiogenesisCell SurvivalRegulatorBiologyNeoplasmsmedicineHumansNuclear proteinSelection GeneticTranscription factorG alpha subunitRegulation of gene expressionHelix-Loop-Helix MotifsNuclear ProteinsHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaDNA-Binding ProteinsGene Expression Regulation NeoplasticCell Transformation NeoplasticGlucoseOncologyTumor progressionImmunologyCancer researchDisease ProgressionHypoxia-Inducible Factor 1medicine.symptomTranscription FactorsThe oncologist
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HIF-1 is involved in the negative regulation of AURKA expression in breast cancer cell lines under hypoxic conditions

2013

Numerous microarray-based gene expression studies performed on several types of solid tumors revealed significant changes in key genes involved in progression and regulation of the cell cycle, including AURKA that is known to be overexpressed in many types of human malignancies. Tumor hypoxia is associated with poor prognosis in several cancer types, including breast cancer (BC). Since hypoxia is a condition that influences the expression of many genes involved in tumorigenesis, proliferation, and cell cycle regulation, we performed a microarray-based gene expression analysis in order to identify differentially expressed genes in BC cell lines exposed to hypoxia. This analysis showed that h…

Cancer ResearchSettore MED/06 - Oncologia MedicaDown-RegulationBreast NeoplasmsBiologymedicine.disease_causeAURKA Breast cancer Cell cycle HIF-1a HypoxiaCell Line TumorGene expressionTranscriptional regulationmedicineHumansPromoter Regions GeneticAurora Kinase ARegulation of gene expressionGene knockdownTumor hypoxiaCell cycleHypoxia (medical)Hypoxia-Inducible Factor 1 alpha SubunitMolecular biologyCell HypoxiaGene Expression Regulation NeoplasticOncologyGene Knockdown TechniquesCancer researchFemalemedicine.symptomCarcinogenesisBreast Cancer Research and Treatment
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