Search results for "Transforming growth factor"

showing 10 items of 294 documents

Coexpression of extracellular matrix glycoproteins undulin and tenascin in human autosomal dominant polycystic kidney disease.

1993

Autosomal dominant polycystic kidney disease (ADPKD) is the most common entity of cystic diseases of the kidney leading to end-stage renal insufficiency. Changes in extracellular matrix (ECM) are regarded to be an important pathogenic factor connected with the genes assumed to be responsible for human ADPKD. In order to assess the biological significance of altered expression and deposition of ECM glycoproteins for human ADPKD at molecular levels fresh-frozen tissue from ADPKD kidneys, fetal kidneys and normal adult kidneys were comparatively tested by immunohistochemistry for the presence of multifunctional ECM glycoproteins undulin, tenascin and fibronectin, interstitial collagen types I,…

Pathologymedicine.medical_specialtyCell Adhesion Molecules NeuronalAutosomal dominant polycystic kidney diseaseTenascinGene ExpressionKidneyExtracellular matrixFetusLamininTransforming Growth Factor betamedicineHumansRNA MessengerCells CulturedGlycoproteinsBasement membraneKidneyExtracellular Matrix Proteinsbiologyurogenital systemTenascinmedicine.diseasePolycystic Kidney Autosomal DominantImmunohistochemistryEpitheliumCell biologyFibronectinsFibronectinmedicine.anatomical_structurebiology.proteinCollagenLamininNephron
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Dupuytren's contracture: an update of biomolecular aspects and therapeutic perspectives.

2005

The so-called fibrogenic cytokines, able to induce the growth of fibroblasts and their differentiation into myofibroblasts and to stimulate their production of extracellular matrix, are involved in the genesis of Dupuytren’s contracture. Although many studies have been made of biomolecular aspects of palmar fibromatosis, practical applications from them are still far from imminent because of the real difficulty of blocking their action in vivo, even in a chronic, progressive lesion such as Dupuytren’s disease. Consequently, surgical excision of the palmar fascia still remains the treatment of choice.

Pathologymedicine.medical_specialtyGENETIC SUSCEPTIBILITYFIBRONECTINBioinformaticsDISEASEExtracellular matrixTransforming Growth Factor betamedicineFIBROSISHumansGenetic Predisposition to DiseaseDupuytren's contracturePlatelet-Derived Growth FactorTransplantationEpidermal Growth Factorbusiness.industryGROWTH-FACTOR-BETANONOPERATIVE TREATMENTSTEROIDSFibromatosisGranulocyte-Macrophage Colony-Stimulating FactorTissue Inhibitor of MetalloproteinasesFasciaASSOCIATIONmedicine.diseaseHandCOLLAGENFasciotomyFibronectinsbody regionsDupuytren Contracturemedicine.anatomical_structureMetalloproteasesSurgeryContracturemedicine.symptombusinessPalmar fasciaMyofibroblastMATRIXPalmar FibromatosisJournal of hand surgery (Edinburgh, Scotland)
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Transfer of the active form of transforming growth factor-beta 1 gene to newborn rat lung induces changes consistent with bronchopulmonary dysplasia.

2003

Bronchopulmonary dysplasia is a chronic lung disease of premature human infancy that shows pathological features comprising varying sized areas of interstitial fibrosis in association with distorted large alveolar spaces. We have previously shown that transfer of active transforming growth factor (TGF)-beta 1 (AdTGF beta 1(223/225)) genes by adenovirus vector to embryonic lungs results in inhibition of branching morphogenesis and primitive peripheral lung development, whereas transfer to adult lungs results in progressive interstitial fibrosis. Herein we show that transfer of TGF-beta1 to newborn rat pups results in patchy areas of interstitial fibrosis developing throughout a period of 28 …

Pathologymedicine.medical_specialtymedicine.medical_treatmentPulmonary FibrosisPathology and Forensic MedicineRats Sprague-DawleyTransforming Growth Factor beta1FibrosisTransforming Growth Factor betaPulmonary fibrosismedicineAnimalsHumansLungBronchopulmonary DysplasiaLungbiologyRespiratory diseaseGene Transfer TechniquesInfant NewbornTransforming growth factor betarespiratory systemmedicine.diseaseRatsDisease Models AnimalCytokinemedicine.anatomical_structureBronchopulmonary dysplasiaAnimals Newbornbiology.proteinAnimal ModelTransforming growth factorThe American journal of pathology
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Contribution of sinusoidal endothelial liver cells to liver fibrosis: expression of transforming growth factor-beta 1 receptors and modulation of pla…

1993

Transforming growth factor-beta 1 is an important cytokine in the pathophysiology of liver fibrosis, stimulating the production of extracellular matrix. Whether this cytokine can also control the degradation of matrix proteins in liver cells has not been investigated. Because plasmin is an important protease for the degradation of matrix glycoproteins, we investigated whether sinusoidal endothelial liver cells could contribute to fibrosing liver disease through the modulation of plasmin-generating enzymes in response to transforming growth factor-beta 1. Sinusoidal endothelial cells from guinea pig liver were investigated in pure monolayer culture. Using 125I-labelled transforming growth fa…

PlasminGuinea PigsBiologyLiver Cirrhosis Experimental03 medical and health sciencesPlasminogen Activators0302 clinical medicineCell surface receptorTransforming Growth Factor betaPlasminogen Activator Inhibitor 1medicineAnimalsFibrinolysinCells Cultured030304 developmental biology0303 health sciencesHepatology3. Good healthCell biologyFibronectinEndothelial stem cellBiochemistryLiverTransforming growth factor beta 3Cell culturebiology.protein030211 gastroenterology & hepatologyFemaleEndothelium VascularPlasminogen activatorReceptors Transforming Growth Factor betamedicine.drugTransforming growth factorHepatology (Baltimore, Md.)
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Diverse cell surface protein ectodomains are shed by a system sensitive to metalloprotease inhibitors.

1996

The extracellular domains of a diverse group of membrane proteins are shed in response to protein kinase C activators such as phorbol 12-myristate 13-acetate (PMA). The lack of sequence similarity in the cleavage sites suggests the involvement of many proteases of diverse specificity in this process. However, a mutant Chinese hamster ovary cell line recently isolated for being defective in PMA-activated shedding of the membrane-anchored growth factor transforming growth factor alpha precursor (proTGF-alpha) is concomitantly defective in the shedding of many other unrelated membrane proteins. Here we show that independent mutagenesis and selection experiments yield shedding mutants having th…

ProteasesCellCHO CellsBiologyHydroxamic AcidsTransfectionBiochemistryAmyloid beta-Protein PrecursorAntigens CDCricetinaemedicineAnimalsProtease InhibitorsL-SelectinProtein PrecursorsCell adhesionMolecular BiologyProtein kinase CMetalloproteinaseChinese hamster ovary cellCell MembraneGenetic Complementation TestMembrane ProteinsMetalloendopeptidasesCell BiologyReceptors InterleukinTransforming Growth Factor alphaReceptors Interleukin-6Cell biologyKineticsmedicine.anatomical_structurePhenotypeEctodomainMembrane proteinMutagenesisTetradecanoylphorbol AcetatePhenanthrolinesThe Journal of biological chemistry
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Apoptosis in liver disease

2001

A variety of biological functions are regulated through extracellular signals. Amongst the best studied examples is growth control, which is achieved by the regulatory function of growth factors. In recent years it has become apparent that cell death (apoptosis) is controlled in a similar fashion. Apoptosis, firstly a morphologically defined process, is a highly controlled type of cell death that plays a critical role in embryonic development, deletion of autoreactive T-cells and adult tissue homoeostasis. There is increasing evidence that derangement of the apoptotic program is the underlying cause of a series of diseases including liver diseases. The deadly program can be initiated by lig…

ProteasesProgrammed cell deathApoptosisLigandsReceptors Tumor Necrosis FactorFas ligandTransforming Growth Factor beta1Antigens CDTransforming Growth Factor betaExtracellularAnimalsHumansfas ReceptorCaspaseHepatologybiologyLiver DiseasesGastroenterologyFas receptorCell biologyBiochemistryReceptors Tumor Necrosis Factor Type IApoptosisCaspasesbiology.proteinIntracellularEuropean Journal of Gastroenterology & Hepatology
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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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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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