Search results for "Growth factor"

showing 10 items of 1300 documents

Epithelial-mesenchymal communication in the pathogenesis of chronic asthma.

2005

Although Th-2-mediated inflammation is a key therapeutic target in asthma, its relationship to altered structure and functions of the airways is largely unknown. In addition to inflammation, asthma is a disorder involving the airway epithelium that is more vulnerable to environmental injury and responds to this by impaired healing. This establishes a chronic wound scenario that is capable of sustaining chronic inflammation as well as remodeling. This response occurs as a consequence of activation of the epithelial-mesenchymal unit, involving reciprocal activities of growth factors belonging to the fibroblast growth factor, epidermal growth factor, and transforming growth factor-beta familie…

Pulmonary and Respiratory MedicineChronic woundInflammationBiologyFibroblast growth factorPathogenesisTh2 CellsEpidermal growth factormedicineHumansGrowth Substancesasthma InflammationAsthmaInflammationWound HealingMesenchymal stem cellModels ImmunologicalEpithelial CellsMuscle SmoothFibroblastsmedicine.diseaseAsthmarespiratory tract diseasesImmunologyChronic DiseaseRespiratory Physiological PhenomenaRespiratory epitheliumCytokinesmedicine.symptom
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Roflumilast N-oxide inhibits bronchial epithelial to mesenchymal transition induced by cigarette smoke in smokers with COPD.

2014

Abstract Background Epithelial to mesenchymal transition (EMT) is under discussion as a potential mechanism of small airway remodelling in COPD. In bronchial epithelium of COPD and smokers markers of EMT were described. In vitro, EMT may be reproduced by exposing well-differentiated human bronchial epithelial cells (WD-HBEC) to cigarette smoke extract (CSE). EMT may be mitigated by an increase in cellular cAMP. Objective This study explored the effects of roflumilast N-oxide, a PDE4 inhibitor on CSE-induced EMT in WD-HBEC and in primary bronchial epithelial cells from smokers and COPD in vitro. Methods WD-HBEC from normal donors were stimulated with CSE (2.5%) for 72 h in presence of roflum…

Pulmonary and Respiratory MedicineCyclopropanesMalePathologymedicine.medical_specialtyEpithelial-Mesenchymal TransitionAminopyridinesVimentinApoptosisBronchiEnzyme-Linked Immunosorbent AssayRespiratory MucosaIn Vitro TechniquesTransforming Growth Factor beta1Pulmonary Disease Chronic ObstructiveAnnexinSmokemedicineCyclic AMPHumansPharmacology (medical)Epithelial–mesenchymal transitiontabac efectes fisiològicsRoflumilastAgedchemistry.chemical_classificationReactive oxygen speciesbiologybusiness.industryBiochemistry (medical)Mesenchymal stem cellSmokingNOX4Epithelial CellsfarmacologiaMiddle Agedrespiratory tract diseaseschemistryApoptosisBenzamidesbiology.proteinCancer researchFemalePhosphodiesterase 4 Inhibitorspulmons malalties obstructivesbusinessReactive Oxygen Speciesmedicine.drugPulmonary pharmacologytherapeutics
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Modulation of IL-1?, IL-6, IL-8, TNF-?, and TGF-? secretions by alveolar macrophages under NO2 exposure

2004

Activated alveolar macrophages (AMs) secrete interleukine (IL)1β, IL-6, IL-8, tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β), whose inflammatory and fibroblast-activating characteristics may play a role in the maintenance of pulmonary inflammatory processes and subsequent fibrosis. Human AMs were transferred to a gas cylinder and exposed to NO2 in concentrations ranging from 0.1 to 0.5 ppm in synthetic air for 30 min at 37°C. AMs were fixed on a polycarbonate membrane and placed on culture medium. A culture was established, with the exposed AM (nonstimulated or stimulated with 1 μg/ml lipopolysaccharide [LPS]), and the remaining cells were used to determine the cy…

Pulmonary and Respiratory MedicineLipopolysaccharideBiologymedicine.diseaseAndrologychemistry.chemical_compoundchemistryFibrosisImmunologymedicinebiology.proteinTumor necrosis factor alphaTrypan blueInterleukin 8CytotoxicityInterleukin 6Transforming growth factorLung
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Impact of T-cell-mediated immune response on xenogeneic heart valve transplantation: short-term success and mid-term failure.

2017

Objectives Allogeneic frozen cryopreserved heart valves (allografts or homografts) are commonly used in clinical practice. A major obstacle for their application is the limited availability in particular for paediatrics. Allogeneic large animal studies revealed that alternative ice-free cryopreservation (IFC) results in better matrix preservation and reduced immunogenicity. The objective of this study was to evaluate xenogeneic (porcine) compared with allogeneic (ovine) IFC heart valves in a large animal study. Methods IFC xenografts and allografts were transplanted in 12 juvenile merino sheep for 1-12 weeks. Immunohistochemistry, ex vivo computed tomography scans and transforming growth fa…

Pulmonary and Respiratory MedicinePathologymedicine.medical_specialtySwineT-Lymphocytes0206 medical engineering02 engineering and technology030204 cardiovascular system & hematologySpectrum Analysis RamanCryopreservation03 medical and health sciences0302 clinical medicineTransforming Growth Factor betaImmunopathologyTranslational ResearchMedicineAnimalsBioprosthesisImmunity CellularSheepbiologybusiness.industryImmunogenicityGeneral MedicineTransforming growth factor beta020601 biomedical engineeringHeart ValvesTransplantationHeart valve transplantationHeart Valve Prosthesisbiology.proteinSurgeryCardiology and Cardiovascular MedicinebusinessTomography X-Ray ComputedElastinEx vivoEuropean journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery
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CD34+ progenitor to endothelial cell transition in post-pneumonectomy angiogenesis.

2012

In many species, pneumonectomy triggers compensatory lung growth that results in an increase not only in lung volume, but also in alveolar number. Whether the associated alveolar angiogenesis involves the contribution of blood-borne progenitor cells is unknown. To identify and characterize blood-borne progenitor cells contributing to lung growth after pneumonectomy in mice, we studied wild-type and wild-type/green fluorescence protein (GFP) parabiotic mice after left pneumonectomy. Within 21 days of pneumonectomy, a 3.2-fold increase occurred in the number of lung endothelial cells. This increase in total endothelial cells was temporally associated with a 7.3-fold increase in the number of …

Pulmonary and Respiratory MedicineTranscriptional ActivationPathologymedicine.medical_specialtyTime FactorsAngiogenesisCellular differentiationClinical BiochemistryGreen Fluorescent ProteinsCD34Neovascularization PhysiologicAntigens CD34Mice TransgenicBiologyMiceVasculogenesisCell MovementmedicineAnimalsRegenerationProgenitor cellPneumonectomyMolecular BiologyLungCell ProliferationStem CellsEndothelial CellsCell DifferentiationCell BiologyArticlesEndothelial stem cellVascular endothelial growth factor BMice Inbred C57BLGene Expression RegulationCancer researchStem cellAmerican journal of respiratory cell and molecular biology
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Moving osimertinib to first-line: the right “strategy” in the chessboard of epidermal growth factor receptor-mutated non-small cell lung cancer?

2018

In the N Engl J Med , Soria and colleagues have recently reported the results of the phase III randomized FLAURA trial (1), comparing osimertinib with first generation epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) gefitinib or erlotinib in treatment-naive patients with advanced non-small cell lung cancer (NSCLC) and activating EGFR -mutations.

Pulmonary and Respiratory Medicinebiologybusiness.industryKinasemedicine.diseaserespiratory tract diseases03 medical and health sciences0302 clinical medicineGefitinibEditorialEpidermal growth factor030220 oncology & carcinogenesisCancer researchbiology.proteinMedicineOsimertinibHuman medicine030212 general & internal medicineEpidermal growth factor receptorNon small cellErlotinibbusinessLung cancerneoplasmsmedicine.drug
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Circulating haemopoietic and endothelial progenitor cells are decreased in COPD

2006

Circulating CD34+ cells are haemopoietic progenitors that may play a role in tissue repair. No data are available on circulating progenitors in chronic obstructive pulmonary disease (COPD). Circulating CD34+ cells were studied in 18 patients with moderate-to-severe COPD (age: mean+/-sd 68+/-8 yrs; forced expiratory volume in one second: 48+/-12% predicted) and 12 controls, at rest and after endurance exercise. Plasma concentrations of haematopoietic growth factors (FMS-like tyrosine kinase 3 (Flt3) ligand, kit ligand), markers of hypoxia (vascular endothelial growth factor (VEGF)) and stimulators of angiogenesis (VEGF, hepatocyte growth factor (HGF)) and markers of systemic inflammation (tu…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyAngiogenesisCD34Antigens CD34cd34Settore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - Fisiologiachronic obstructive pulmonary diseaseimmunologyPulmonary Disease Chronic Obstructivecd34+ cellscd34+cellschemistry.chemical_compoundantigensbloodstem cellsInternal medicinegrowth factorsmiddle agedMedicineProgenitor cellhumansCD34+ cells chronic obstructive pulmonary disease exercise growth factors hypoxiacell countpulmonary diseaseCOPDchronic obstructiveexercisehypoxiabusiness.industryaged; antigens; blood; cd34; cd34+ cells; cd34+cells; cell count; chronic obstructive; chronic obstructive pulmonary disease; endothelial cells; exercise; growth factors; hematopoietic stem cells; humans; hypoxia; immunology; middle aged; pulmonary disease; stem cellsHypoxia (medical)medicine.diseaseendothelial cellshematopoietic stem cellsEndothelial stem cellVascular endothelial growth factoragedEndocrinologychemistryHepatocyte growth factormedicine.symptombusinessmedicine.drugEuropean Respiratory Journal
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Aclidinium inhibits human lung fibroblast to myofibroblast transition

2011

Background Fibroblast to myofibroblast transition is believed to contribute to airway remodelling in lung diseases such as asthma and chronic obstructive pulmonary disease. This study examines the role of aclidinium, a new long-acting muscarinic antagonist, on human fibroblast to myofibroblast transition. Methods Human bronchial fibroblasts were stimulated with carbachol (10 −8 to 10 −5  M) or transforming growth factor-β1 (TGF-β1; 2 ng/ml) in the presence or absence of aclidinium (10 −9 to 10 −7  M) or different drug modulators for 48 h. Characterisation of myofibroblasts was performed by analysis of collagen type I and α-smooth muscle actin (α-SMA) mRNA and protein expression as well as α…

Pulmonary and Respiratory Medicinemedicine.medical_specialtyCarbacholChronic Obstructive Pulmonary DiseaseBronchiMuscarinic AntagonistsBiologyCholinergic AgonistsCollagen Type ITransforming Growth Factor beta1Downregulation and upregulationWestern blotanticholinergicCell MovementInternal medicinemedicineCOPDHumans1506RNA MessengerAutocrine signallingFibroblastMyofibroblastsCells CulturedCell Proliferationmedicine.diagnostic_testDose-Response Relationship Drugairway epitheliumCell Differentiationasthmainterstitial fibrosisFibroblastsAdenosineMolecular biologymyofibroblastActinsUp-RegulationEndocrinologymedicine.anatomical_structurePhosphorylationFibroblastCarbacholMyofibroblastmedicine.drugTropanesThorax
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Longevity: epigenetic and biomolecular aspects

2015

AbstractMany aging theories and their related molecular mechanisms have been proposed. Simple model organisms such as yeasts, worms, fruit flies and others have massively contributed to their clarification, and many genes and pathways have been associated with longevity regulation. Among them, insulin/IGF-1 plays a key and evolutionary conserved role. Interestingly, dietary interventions can modulate this pathway. Calorie restriction (CR), intermittent fasting, and protein and amino acid restriction prolong the lifespan of mammals by IGF-1 regulation. However, some recent findings support the hypothesis that the long-term effects of diet also involve epigenetic mechanisms. In this review, w…

QH301-705.5media_common.quotation_subjectmedicine.medical_treatmentCalorie restrictionved/biology.organism_classification_rank.speciesBiologyGeneral Biochemistry Genetics and Molecular BiologyEpigenesis GeneticCellular and Molecular NeuroscienceDietary interventionslongevityIntermittent fastingmedicineAnimalsHumansInsulinEpigeneticsBiology (General)Insulin-Like Growth Factor IModel organismGenemedia_commonGeneticsepigeneticsAnimalved/biologyInsulinLongevityGeneral Medicinecaloric restrictionepigeneticMetabolic Networks and PathwaysHumanBiomolecular Concepts
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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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