Search results for "eta1"

showing 10 items of 133 documents

The Late Endosomal Adaptor Molecule p14 (LAMTOR2) Regulates TGFβ1-Mediated Homeostasis of Langerhans Cells

2014

Langerhans cells (LCs), a sub-population of dendritic cells (DCs) in the skin, participate in the regulation of immunity and peripheral tolerance. The adaptor molecule p14 is part of the late endosomal/lysosomal adaptor and mitogen-activated protein kinase and mammalian target of rapamycin (mTOR) activator/regulator (LAMTOR) complex, which mediates the activation of lysosome-associated extracellular signaling regulated kinase (ERK) and the mTOR cascade. In previous work, we demonstrated that CD11c-specific deficiency of p14 disrupts LC homeostasis by affecting the LAMTOR-mediated ERK and mTOR signaling. In this study, we extended our analysis on p14 deficiency specifically in LCs. Langerin-…

MAPK/ERK pathwayMaleMAP Kinase Signaling SystemReceptor Transforming Growth Factor-beta Type IDown-Regulationchemical and pharmacologic phenomenaEndosomesDermatologyBiologyProtein Serine-Threonine KinasesDermatitis ContactBiochemistryArticleImmune toleranceImmunophenotypingTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationCell MovementImmune ToleranceAnimalsHomeostasisProtein kinase AMolecular BiologyPI3K/AKT/mTOR pathway030304 developmental biologySkin0303 health sciencesintegumentary systemKinaseReceptor Transforming Growth Factor-beta Type IIPeripheral toleranceProteinshemic and immune systemsCell BiologyMice Mutant StrainsCell biologyCD11c AntigenLangerhans CellsFemaleReceptors Transforming Growth Factor beta030215 immunologyTransforming growth factorJournal of Investigative Dermatology
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Heat shock proteins in fibrosis and wound healing: Good or evil?

2014

Heat shock proteins (HSPs) are key regulators of cell homeostasis, and their cytoprotective role has been largely investigated in the last few decades. However, an increasing amount of evidence highlights their deleterious effects on several human pathologies, including cancer, in which they promote tumor cell survival, proliferation and drug resistance. Therefore, HSPs have recently been suggested as therapeutic targets for improving human disease outcomes. Fibrotic diseases and cancer share several properties; both pathologies are characterized by genetic alterations, uncontrolled cell proliferation, altered cell interactions and communication and tissue invasion. The discovery of new HSP…

MAPK/ERK pathwayPulmonary FibrosisCellApoptosisBiologyCell Physiological PhenomenaTransforming Growth Factor beta1PathogenesisFibrosisNeoplasmsHeat shock proteinmedicineHumansHSP70 Heat-Shock ProteinsPharmacology (medical)HSP90 Heat-Shock ProteinsHSP110 Heat-Shock ProteinsHSP47 Heat-Shock ProteinsHeat-Shock ProteinsPharmacologyWound HealingCell growthCancerEndomyocardial Fibrosismedicine.diseaseFibrosisHeat-Shock Proteins Smallmedicine.anatomical_structureImmunologyCancer researchCollagenWound healingPharmacology & Therapeutics
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Keratinocyte-Derived Granulocyte-Macrophage Colony Stimulating Factor Accelerates Wound Healing: Stimulation of Keratinocyte Proliferation, Granulati…

2001

Chronic, nonhealing wounds represent a major clinical challenge to practically all disciplines in modern medicine including dermatology, oncology, surgery, and hematology. In skin wounds, granulocyte-macrophage colony stimulating factor (GM-CSF) is secreted by keratinocytes shortly after injury and mediates epidermal cell proliferation in an autocrine manner. Many other cells involved in wound healing including macrophages, lymphocytes, fibroblasts, endothelial cells, and dendritic cells synthesize GM-CSF and/or are targets of this cytokine. Therefore, GM-CSF is a pleiotropic cytokine evoking complex processes during wound repair. Despite this complexity and the scarcity of mechanistic unde…

Macrophage colony-stimulating factorKeratinocytesMalemedicine.medical_treatmentGene ExpressionMitosisNeovascularization PhysiologicMice TransgenicDermatologytransgenic miceBiologyBiochemistryProinflammatory cytokineTransforming Growth Factor beta1MiceTransforming Growth Factor betamedicineAnimalsRNA MessengerAutocrine signallingMolecular BiologySkinWound Healingintegumentary systemGranulation tissueGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFCell BiologyUp-RegulationCytokinemedicine.anatomical_structureGranulocyte macrophage colony-stimulating factorImmunologyModels AnimalCancer researchCarcinogensGranulation TissueCytokinesTetradecanoylphorbol AcetateFemaleKeratinocyteWound healingmedicine.drugJournal of Investigative Dermatology
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β1 integrin signaling promotes neuronal migration along vascular scaffolds in the post-stroke brain

2017

Cerebral ischemic stroke is a main cause of chronic disability. However, there is currently no effective treatment to promote recovery from stroke-induced neurological symptoms. Recent studies suggest that after stroke, immature neurons, referred to as neuroblasts, generated in a neurogenic niche, the ventricular-subventricular zone, migrate toward the injured area, where they differentiate into mature neurons. Interventions that increase the number of neuroblasts distributed at and around the lesion facilitate neuronal repair in rodent models for ischemic stroke, suggesting that promoting neuroblast migration in the post-stroke brain could improve efficient neuronal regeneration. To move t…

Male0301 basic medicineChain migrationlcsh:MedicineExtracellular matrixNeural Stem CellsCell MovementLamininCells CulturedMice KnockoutNeuronslcsh:R5-920Mice Inbred ICRMicroscopy ConfocalTissue ScaffoldsbiologyIntegrin beta1BrainCell migrationGeneral MedicineCell biologyStrokeVasculature-guided migrationFemaleBlood vesselmedicine.symptomlcsh:Medicine (General)Signal TransductionResearch Paperanimal structuresIntegrinMice TransgenicGeneral Biochemistry Genetics and Molecular BiologyLesion03 medical and health sciencesNeuroblastβ1 integrinNeuroblast migrationmedicineAnimalsRegeneration (biology)lcsh:RCoculture TechniquesMicroscopy Electron030104 developmental biologynervous systemAstrocytesImmunologybiology.proteinBlood VesselsLamininEBioMedicine
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Bi-allelic LoF NRROS Variants Impairing Active TGF-β1 Delivery Cause a Severe Infantile-Onset Neurodegenerative Condition with Intracranial Calcifica…

2020

Negative regulator of reactive oxygen species (NRROS) is a leucine-rich repeat-containing protein that uniquely associates with latent transforming growth factor beta-1 (TGF- β1) and anchors it on the cell surface; this anchoring is required for activation of TGF-β1 in macrophages and microglia. We report six individuals from four families with bi-allelic variants in NRROS. All affected individuals had neurodegenerative disease with refractory epilepsy, developmental regression, and reduced white matter volume with delayed myelination. The clinical course in affected individuals began with normal development or mild developmental delay, and the onset of seizures occurred within the first ye…

Male0301 basic medicineInflammationBiologyintracranial calcificationneuroinflammationTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineReportTGF-β1NRROSGeneticsmedicineHumansAllelesGenetics (clinical)NeuroinflammationBrain DiseasesMicrogliaMacrophagesNeurodegenerationneurodegenerationCalcinosisGenetic VariationInfantNeurodegenerative Diseasesmedicine.diseaseNFKB1Latent TGF-beta binding proteinHEK293 Cells030104 developmental biologymedicine.anatomical_structureLatent TGF-beta Binding ProteinsImmunologyKnockout mouseFemaleMicrogliamutationmedicine.symptomDevelopmental regression030217 neurology & neurosurgeryThe American Journal of Human Genetics
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Sequential BMP7/TGF-β1 signaling and microbiota instruct mucosal Langerhans cell differentiation

2018

Capucha et al. demonstrate that mucosal Langerhans cell (LC) differentiation from pre–dendritic cells and monocytes involves consecutive BMP7 and TGF-β1 signaling in separate anatomical locations. Moreover, mucosal microbiota regulates the development of LCs that in turn shape microbial and immunological homeostasis.

Male0301 basic medicineLangerhans cellBone Morphogenetic Protein 7ImmunologyReceptor Transforming Growth Factor-beta Type IBiologyArticle311Transforming Growth Factor beta1Mice03 medical and health sciencesDownregulation and upregulation319Langerhans cell differentiationmedicineAnimalsHumansImmunology and AllergyLectins C-TypeImmunity MucosalResearch ArticlesBone Morphogenetic Protein Receptors Type IMice KnockoutLamina propriaintegumentary systemMicrobiotaStem CellsMouth MucosaMucous membraneCell DifferentiationEpitheliumUp-RegulationCell biologyMice Inbred C57BLBone morphogenetic protein 7Mannose-Binding Lectins030104 developmental biologymedicine.anatomical_structureLangerhans CellsAntigens SurfaceSignal transductionTranscriptomeSignal TransductionJournal of Experimental Medicine
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TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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Inhibition of cancer growth by resveratrol is related to its low bioavailability.

2002

The relationship between resveratrol (RES) bioavalability and its effect on tumor growth was investigated. Tissue levels of RES were studied after i.v. and oral administration of trans-resveratrol (t-RES) to rabbits, rats, and mice. Half-life of RES in plasma, after i.v. administration of 20 mg t-RES/kg b.wt., was very short (e.g., 14.4 min in rabbits). The highest concentration of RES in plasma, either after i.v. or oral administration (e.g., 2.6 +/- 1.0 microM in mice 2.5 min after receiving 20 mg t-RES/kg orally), was reached within the first 5 min in all animals studied. Extravascular levels (brain, lung, liver, and kidney) of RES, which paralleled those in plasma, were always1 nmol/g f…

MaleEndotheliumMelanoma ExperimentalBiological AvailabilityVascular Cell Adhesion Molecule-1ResveratrolPharmacologyIn Vitro TechniquesIntegrin alpha4beta1medicine.disease_causeBiochemistrychemistry.chemical_compoundMiceOral administrationPhysiology (medical)StilbenesmedicineCell AdhesionAnimalsTissue DistributionRats Wistarchemistry.chemical_classificationKidneyReactive oxygen speciesCell growthAntineoplastic Agents PhytogenicBioavailabilityRatsMice Inbred C57BLmedicine.anatomical_structurechemistryBiochemistryLiverResveratrolRabbitsOxidative stressCell DivisionHalf-LifeFree radical biologymedicine
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MUC16 Is Overexpressed in Idiopathic Pulmonary Fibrosis and Induces Fibrotic Responses Mediated by Transforming Growth Factor-β1 Canonical Pathway

2021

Several transmembrane mucins have demonstrated that they contribute intracellularly to induce fibrotic processes. The extracellular domain of MUC16 is considered as a biomarker for disease progression and death in IPF patients. However, there is no evidence regarding the signalling capabilities of MUC16 that contribute to IPF development. Here, we demonstrate that MUC16 was overexpressed in the lung tissue of IPF patients (n = 20) compared with healthy subjects (n = 17) and localised in fibroblasts and hyperplastic alveolar type II cells. Repression of MUC16 expression by siRNA-MUC16 transfection inhibited the TGF-β1-induced fibrotic processes such as mesenchymal/ myofibroblast transformati…

MaleMUC16Gene ExpressionIdiopathic pulmonary fibrosis0302 clinical medicineBiology (General)PhosphorylationMyofibroblastsLungSpectroscopytransforming growth factor betabiologyChemistryGeneral MedicineTransfectionMiddle Agedrespiratory systemidiopathic pulmonary fibrosisImmunohistochemistryRespiratory Function TestsComputer Science ApplicationsChemistrymedicine.anatomical_structure030220 oncology & carcinogenesisFemaleDisease SusceptibilityMyofibroblastSignal TransductionQH301-705.5Models BiologicalArticleCatalysisCell LineTransforming Growth Factor beta1Inorganic Chemistry03 medical and health sciencesmedicineHumansPhysical and Theoretical ChemistryFibroblastQD1-999Molecular BiologyAgedCell ProliferationA549 cellOrganic ChemistryMesenchymal stem cellMembrane ProteinsTransforming growth factor betaFibroblastsmedicine.diseaserespiratory tract diseases030228 respiratory systemCA-125 AntigenCase-Control StudiesCancer researchbiology.proteinIdiopathic Pulmonary Fibrosis ; Muc16 ; Transforming Growth Factor BetaBiomarkersTransforming growth factorInternational Journal of Molecular Sciences
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The Role of Transforming Growth Factor-β1 in Airway Inflammation of Childhood Asthma

2013

TGF-beta-targeting structural and inflammatory cells has been implicated in the mechanisms leading to the inflammatory and restructuring processes in asthma, suggesting an impact of TGF-beta1 signaling on the development and persistency of this disease. We investigated the potential early involvement of TGF-beta1 activity in the immunological and molecular mechanisms underlying progression of inflammation in childhood asthma. We evaluated the levels of TGF-beta1 in induced sputum supernatants (ISSs) and the expression of small mother cell against decapentaplegic (Smad) 2 and Smad7 proteins in induced sputum cells (ISCs) from children with intermittent asthma (IA), moderate asthma (MA) and c…

MaleNeutrophilsSmad2 ProteinSMADEosinophilAdrenal Cortex HormoneSeverity of Illness IndexAdrenal Cortex HormonesImmunology and AllergyAge FactorPhosphorylationChildLungNeutrophilAge FactorsBronchodilator Agentsmedicine.anatomical_structureFemalemedicine.symptomCase-Control StudieHumanSignal TransductionGranulocyte activationAdolescentImmunologyAge Factors; Humans; Child; Macrophage-1 Antigen; Adrenal Cortex Hormones; Granulocytes; Neutrophils; Phosphorylation; Eosinophils; Adolescent; Signal Transduction; Male; Severity of Illness Index; Respiratory Mucosa; Asthma; Transforming Growth Factor beta1; Epithelial Cells; Lung; Smad2 Protein; Case-Control Studies; Smad7 Protein; Sputum; Administration Inhalation; Bronchodilator Agents; Cell Line; Female; Cell AdhesionMacrophage-1 AntigenCD18InflammationRespiratory MucosaGranulocyteCell LineSmad7 ProteinTransforming Growth Factor beta1Administration InhalationCell AdhesionmedicineHumansCell adhesionBronchodilator AgentPharmacologyEpithelial Cellbusiness.industrySputumGranulocyteEpithelial CellsEosinophilAsthmaEosinophilsCase-Control StudiesImmunologySputumbusinessGranulocytesInternational Journal of Immunopathology and Pharmacology
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