Search results for "myofibroblast"

showing 10 items of 67 documents

Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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DPP-4 is overexpressed in lung tissue from idiopathic pulmonary patients and activates lung fibroblasts

2020

Background: Idiopathic pulmonary fibrosis (IPF) is a progressive and irreversible form of fibrotic interstitial lung disease, characterized by uncontrolled fibroblast invasion. Dipeptidyl peptidase-4 (DPP-4)/ glucagon-like peptide 1 (GLP-1) system is involved in multiple effects, including cardiac, liver or kidney fibrosis. However, its implication in IPF has not been described. Objective: To analyse the implication of DPP4/GLP1 system in IPF. Methods: Protein expression of DPP4, GLP-1 and GLP-1 receptor was analyzed in lung tissues from 7 IPF patients. TGFβ1-induced fibroblast to myofibroblast transition (FMT), epithelial to mesenchymal transition (EMT) and mesothelial to mesenchymal trans…

Lungbusiness.industrydigestive oral and skin physiologyInterstitial lung diseaserespiratory systemmedicine.diseaserespiratory tract diseasesCTGFIdiopathic pulmonary fibrosismedicine.anatomical_structureSitagliptinCancer researchmedicineEpithelial–mesenchymal transitionbusinessMyofibroblastDipeptidyl peptidase-4medicine.drugIdiopathic interstitial pneumonias
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Potential Involvement of Osteopontin in Inflammatory and Fibrotic Processes in Pulmonary Embolism and Chronic Thromboembolic Pulmonary Hypertension

2019

Background Inflammation and incomplete thrombus resolution leading to obstructive fibrotic remodelling are considered critical mechanisms for the development of chronic thromboembolic pulmonary hypertension (CTEPH) after pulmonary embolism (PE). Osteopontin (OPN) is involved in a variety of biological processes including inflammation and tissue fibrosis. Methods OPN plasma concentrations were measured in 70 CTEPH and 119 PE patients. Tissue material from 6 CTEPH patients removed during pulmonary endarterectomy and murine venous thrombi induced by subtotal ligation of the inferior vena cava in C57BL/6 mice were analysed by (immuno)histochemistry. Results CTEPH patients had higher OPN plasma…

Male0301 basic medicinePathologymedicine.medical_specialtyHypertension Pulmonarymedicine.medical_treatmentInflammationEndarterectomy030204 cardiovascular system & hematologyInferior vena cavaTranslational Research BiomedicalPathogenesisMice03 medical and health sciences0302 clinical medicinestomatognathic systemFibrosisThromboembolismmedicineAnimalsHumansProspective StudiesOsteopontinThrombusMyofibroblastsAgedEndarterectomyInflammationbiologybusiness.industryThrombosisHematologyMiddle AgedPrognosismedicine.diseaseFibrosisPulmonary embolismMice Inbred C57BL030104 developmental biologymedicine.veinChronic Diseasebiology.proteinFemaleOsteopontinmedicine.symptomPulmonary EmbolismbusinessBiomarkersThrombosis and Haemostasis
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Deformation-induced transitional myofibroblasts contribute to compensatory lung growth

2016

In many mammals, including humans, removal of one lung (pneumonectomy) results in the compensatory growth of the remaining lung. Compensatory growth involves not only an increase in lung size, but also an increase in the number of alveoli in the peripheral lung; however, the process of compensatory neoalveolarization remains poorly understood. Here, we show that the expression of α-smooth muscle actin (SMA)—a cytoplasmic protein characteristic of myofibroblasts—is induced in the pleura following pneumonectomy. SMA induction appears to be dependent on pleural deformation (stretch) as induction is prevented by plombage or phrenic nerve transection (P < 0.001). Within 3 days of pneumonectomy, …

Male0301 basic medicinePulmonary and Respiratory MedicinePathologymedicine.medical_specialtyTranscription GeneticPhysiologymedicine.medical_treatmentCompensatory growth (organ)Cell SeparationDeformation (meteorology)BiologyPolymerase Chain Reaction03 medical and health sciencesPneumonectomyPhysiology (medical)medicineAnimalsMyofibroblastsPneumonectomyLungImage CytometryLungGene Expression Regulation DevelopmentalCell Biologyrespiratory systemActinsMice Inbred C57BL030104 developmental biologymedicine.anatomical_structureStress MechanicalSingle-Cell AnalysisMyofibroblastResearch ArticleAmerican Journal of Physiology-Lung Cellular and Molecular Physiology
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Myocardial maladaptation to pressure overload in CB2 receptor-deficient mice

2019

Abstract Background Adaptation to aortic valve stenosis leads to myocardial hypertrophy, which has been associated with inflammation, fibrosis and activation of the endocannabinoid system. Since the endocannabinoid system and the CB2 receptor provide cardioprotection and modulate immune response in experimental ischemia, we investigated the role of CB2 in a mouse model of cardiac pressure overload. Methods Transverse aortic constriction was performed in CB2 receptor-deficient (Cnr2−/−) mice and their wild-type littermates (Cnr2+/+). After echocardiography and Millar left heart catheter hemodynamic evaluation hearts were processed for histological, cellular and molecular analyses. Results Th…

Male0301 basic medicinemedicine.medical_specialtyGenotypeFluorescent Antibody TechniqueBlood PressureCardiomegalyInflammation030204 cardiovascular system & hematologyProinflammatory cytokineReceptor Cannabinoid CB2Mice03 medical and health sciences0302 clinical medicineImmune systemFibrosisInternal medicineVentricular DysfunctionmedicineAnimalsMyocytes CardiacMolecular BiologyMice KnockoutPressure overloadCardioprotectionVentricular RemodelingChemistryMyocardiumHemodynamicsmedicine.diseaseImmunohistochemistryEndocannabinoid systemDisease Models AnimalOxidative Stress030104 developmental biologyEndocrinologyFemaleInflammation Mediatorsmedicine.symptomCardiology and Cardiovascular MedicineMyofibroblastBiomarkersEndocannabinoidsJournal of Molecular and Cellular Cardiology
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Evidence for pleural epithelial-mesenchymal transition in murine compensatory lung growth

2017

In many mammals, including rodents and humans, removal of one lung results in the compensatory growth of the remaining lung; however, the mechanism of compensatory lung growth is unknown. Here, we investigated the changes in morphology and phenotype of pleural cells after pneumonectomy. Between days 1 and 3 after pneumonectomy, cells expressing α-smooth muscle actin (SMA), a cytoplasmic marker of myofibroblasts, were significantly increased in the pleura compared to surgical controls (p < .01). Scanning electron microscopy of the pleural surface 3 days post-pneumonectomy demonstrated regions of the pleura with morphologic features consistent with epithelial-mesenchymal transition (EMT); nam…

MaleB VitaminsThin-Layer Chromatography0301 basic medicinePathologyOrganogenesismedicine.medical_treatmentVimentinBiochemistryMiceSpectrum Analysis Techniques0302 clinical medicineMedicine and Health SciencesElectron MicroscopyRespiratory System ProceduresPneumonectomyLungImage CytometryMicroscopyMultidisciplinarybiologyOrganic CompoundsChromatographic TechniquesQRVitaminsrespiratory systemChemistryPhenotypemedicine.anatomical_structureThoracotomySpectrophotometry030220 oncology & carcinogenesisPhysical SciencesPleuraMedicineScanning Electron MicroscopyMyofibroblastResearch Articlemedicine.medical_specialtyEpithelial-Mesenchymal TransitionImaging TechniquesScienceCompensatory growth (organ)BiotinSurgical and Invasive Medical ProceduresResearch and Analysis Methods03 medical and health sciencesPneumonectomyFluorescence ImagingmedicineAnimalsVimentinEpithelial–mesenchymal transitionLungSurgical ExcisionFluorimetryOrganic ChemistryChemical CompoundsBiology and Life SciencesProteinsrespiratory tract diseasesMice Inbred C57BLCytoskeletal ProteinsPlanar ChromatographyB vitamins030104 developmental biologybiology.proteinMesothelial CellPLOS ONE
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HIF-Overexpression and Pro-Inflammatory Priming in Human Mesenchymal Stromal Cells Improves the Healing Properties of Extracellular Vesicles in Exper…

2021

Extracellular vesicles (EVs) derived from mesenchymal stromal cells (MSCs) have therapeutic potential in the treatment of several immune disorders, including ulcerative colitis, owing to their regenerative and immunosuppressive properties. We recently showed that MSCs engineered to overexpress hypoxia-inducible factor 1-alpha and telomerase (MSC-T-HIF) and conditioned with pro-inflammatory stimuli release EVs (EVMSC-T-HIFC) with potent immunomodulatory activity. We tested the efficacy of EVMSC-T-HIFC to repolarize M1 macrophages (Mφ1) to M2-like macrophages (Mφ2-like) by analyzing surface markers and cytokines and performing functional assays in co-culture, including efferocytosis and T-cel…

MaleCrohn’s diseasemedicine.medical_treatmentimmunomodulationMiceIntestinal mucosaCrohn DiseaseMedicineBiology (General)TelomeraseSpectroscopyCell PolarityGeneral MedicineComputer Science ApplicationsChemistryCytokinemacrophage repolarizationhypoxia-inducible factor 1-alphaCytokinesmesenchymal stromal cellsMyofibroblastGastroenterología y hepatologíaQH301-705.5CatalysisArticleInorganic ChemistryExtracellular VesiclesYoung AdultImmune systemCell AdhesionHuman Umbilical Vein Endothelial CellsAnimalsHumansPhysical and Theoretical ChemistryColitisEfferocytosisQD1-999Molecular BiologyAcute colitisbusiness.industryOrganic ChemistryMesenchymal stem cellMesenchymal Stem Cellsmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitDisease Models AnimalTrinitrobenzenesulfonic AcidCancer researchbusiness
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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 effect of the pro-inflammatory cytokine tumor necrosis factor-alpha on human joint capsule myofibroblasts.

2009

Introduction Previous studies have shown that the number of myoblastically differentiated fibroblasts known as myofibroblasts (MFs) is significantly increased in stiff joint capsules, indicating their crucial role in the pathogenesis of post-traumatic joint stiffness. Although the mode of MFs' function has been well defined for different diseases associated with tissue fibrosis, the underlying mechanisms of their regulation in the pathogenesis of post-traumatic joint capsule contracture are largely unknown. Methods In this study, we examined the impact of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) on cellular functions of human joint capsule MFs. MFs were challenged w…

MalePathologymedicine.medical_treatmentFluorescent Antibody TechniqueGene ExpressionDinoprostExtracellular matrixPathogenesisElbow JointImmunology and AllergyCells CulturedReverse Transcriptase Polymerase Chain ReactionAntibodies MonoclonalMiddle AgedImmunohistochemistryExtracellular MatrixCytokinemedicine.anatomical_structureAntirheumatic AgentsCytokinesTumor necrosis factor alphaFemaleHip Jointmedicine.symptomInflammation MediatorsMyofibroblastmusculoskeletal diseasesmedicine.medical_specialtyanimal structuresContractureDiclofenacImmunologyBlotting Westernmacromolecular substancesBiologyCollagen Type IDinoprostoneRheumatologyJoint capsuleResearch articlemedicineHumansAgedCell ProliferationCyclooxygenase 2 InhibitorsTumor Necrosis Factor-alphaProstaglandins FFibroblastsActinsInfliximabCyclooxygenase 2Joint stiffnessContractureJoint CapsuleArthritis researchtherapy
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Vascular effects of sildenafil in patients with pulmonary fibrosis and pulmonary hypertension: an ex vivo/in vitro study

2015

Sildenafil improves the 6-min walking distance in patients with idiopathic pulmonary fibrosis (IPF) and right-sided ventricular systolic dysfunction.We analysed the previously unexplored role of sildenafil on vasoconstriction and remodelling of pulmonary arteries from patients with IPF and pulmonary hypertension (PH) ex vivo. Pulmonary arteries from 18 donors without lung disease, nine IPF, eight PH+IPF and four PH patients were isolated to measure vasodilator and anti-contractile effects of sildenafil in isometric organ bath. Ventilation/perfusion was explored in an animal model of bleomycin lung fibrosis.Sildenafil relaxed serotonin (5-HT) pre-contracted pulmonary arteries in healthy dono…

MalePulmonary FibrosisVasodilator AgentsVasodilation030204 cardiovascular system & hematologyPulmonary Disease Chronic ObstructiveIdiopathic pulmonary fibrosischemistry.chemical_compound0302 clinical medicinePulmonary fibrosisMyofibroblastsLungrespiratory systemExtracellular Matrixmedicine.anatomical_structurecardiovascular systemCardiologymedicine.symptomSignal TransductionPulmonary and Respiratory MedicineSerotoninmedicine.medical_specialtyEndotheliumSildenafilHypertension PulmonaryMyocytes Smooth MusclePulmonary ArterySildenafil CitrateTransforming Growth Factor beta1Bleomycin03 medical and health sciencesmedicine.arteryInternal medicinemedicineAnimalsHumansRats Wistarbusiness.industryFibroblastsmedicine.diseasePulmonary hypertensionRatsrespiratory tract diseasesDisease Models Animal030228 respiratory systemchemistryVasoconstrictionPulmonary arteryEndothelium VascularbusinessVasoconstrictionEuropean Respiratory Journal
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