Search results for "Transforming Growth Factor beta1"

showing 10 items of 72 documents

Notch-1 decreased expression contributes to leptin receptor downregulation in nasal epithelium from allergic turbinates

2019

Abstract BACKGROUND: Allergic rhinitis is characterized by a remodeling of nasal epithelium. Since the Notch and TGF-β signaling pathways are known to be involved in cell differentiation and remodeling processes and leptin adipokine has already been identified as a marker for homeostasis in human bronchial and nasal epithelial cells of asthmatics, roles played by these pathways have been investigated for chronic allergic rhinitis. METHODS: The leptin/leptin receptor expression has been investigated in a study with 40 biopsies from allergic (AR, n = 18) and non-allergic (C, n = 22) inferior turbinates, using immunohistochemistry, immunofluorescence staining and RT-PCR. In addition, extracts …

0301 basic medicineAdultLeptinMalemedicine.medical_specialtyBiopsyPrimary Cell CultureAdipokineTurbinatesCell LineTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineDownregulation and upregulationInternal medicinemedicineHomeostasisHumansRNA MessengerReceptor Notch1610 Medicine & healthReceptorMolecular BiologyNotch 1Leptin receptorChemistryLeptindigestive oral and skin physiologyEpithelial CellsMiddle AgedRhinitis AllergicAllergic rhinitis Epithelium Leptin NotchEpitheliumNasal Mucosa030104 developmental biologyEndocrinologymedicine.anatomical_structureGene Expression Regulation030220 oncology & carcinogenesisCase-Control StudiesMolecular MedicineReceptors LeptinFemaleSignal transductionSignal Transduction
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Arrangement of myofibroblastic and smooth muscle-like cells in superficial peritoneal endometriosis and a possible role of transforming growth factor…

2018

Purpose: Superficial peritoneal endometriotic (pEM) lesions are composed of endometrial glands and stroma, in addition to a third component—myofibroblasts and smooth muscles (SM)-like cells. The latter develops secondary to a metaplasia. In this study, we characterised the third component cells in pEM according to differentiation markers in different micro-compartments. Furthermore, a possible effect of TGFβ1 on myofibroblastic metaplasia in endometriotic epithelial cells was studied. Methods: Seventy-six premenopausal patients were included. Peritoneal biopsies were excised from EM patients (n = 23), unaffected peritoneum (peritoneum from EM patients but without EM components, n = 5/23) an…

0301 basic medicineAdultPathologymedicine.medical_specialtyCalponinEndometriosisPeritoneal DiseasesTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineStromaPeritoneumMetaplasiamedicineHumansEndometriosiMyofibroblastsMyofibroblastMetaplasia030219 obstetrics & reproductive medicinebiologybusiness.industryPeritoneal endometriosiPeritoneal fluidTGFβ1Obstetrics and GynecologyCell DifferentiationMuscle SmoothGeneral MedicineTransforming growth factor beta030104 developmental biologymedicine.anatomical_structurePeritoneal Diseasebiology.proteinSmooth muscle-like cellDesminFemalemedicine.symptomPeritoneumbusinessMyofibroblastMyofibroblastic metaplasiaHumanArchives of gynecology and obstetrics
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Cyclic pentapeptide cRGDfK enhances the inhibitory effect of sunitinib on TGF-β1-induced epithelial-to-mesenchymal transition in human non-small cell…

2020

AbstractIn human lung cancer progression, the EMT process is characterized by the transformation of cancer cells into invasive forms that migrate to other organs. Targeting to EMT-related molecules is emerging as a novel therapeutic approach for the prevention of lung cancer cell migration and invasion. Traf2- and Nck-interacting kinase (TNIK) has recently been considered as an anti-proliferative target molecule to regulate the Wnt signaling pathway in several types of cancer cells. In the present study, we evaluated the inhibitory effect of a tyrosine kinase inhibitor sunitinib and the integrin-αVβ3targeted cyclic peptide (cRGDfK) on EMT in human lung cancer cells. Sunitinib strongly inhib…

0301 basic medicineCell signalingIntegrinsLung NeoplasmsProtein ExpressionCancer TreatmentSmad ProteinsSignal transductionLung and Intrathoracic TumorsTyrosine-kinase inhibitorAdenosine Triphosphate0302 clinical medicineCarcinoma Non-Small-Cell LungCatalytic DomainAntineoplastic Combined Chemotherapy ProtocolsMedicine and Health SciencesSunitinibWnt Signaling PathwayWNT Signaling CascadeMultidisciplinarySunitinibChemistryQRWnt signaling pathwaySignaling cascadesDrug SynergismExtracellular MatrixMolecular Docking SimulationOncology030220 oncology & carcinogenesisMedicineCellular Structures and OrganellesSignal transductionResearch Articlemedicine.drugCell biologySignal InhibitionEpithelial-Mesenchymal TransitionCell Survivalmedicine.drug_classScienceSMAD signalingProtein Serine-Threonine KinasesResearch and Analysis MethodsPeptides CyclicTransforming Growth Factor beta103 medical and health sciencesCell Line TumorGene Expression and Vector TechniquesCell AdhesionBiomarkers TumormedicineHumansNeoplasm InvasivenessEpithelial–mesenchymal transitionMolecular Biology TechniquesLung cancerMolecular BiologyA549 cellMolecular Biology Assays and Analysis TechniquesBiology and life sciencesCancers and NeoplasmsIntegrin alphaVbeta3medicine.diseaseNon-Small Cell Lung Cancer030104 developmental biologyTGF-beta signaling cascadeA549 CellsTNIKCancer cellCancer researchPLOS ONE
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Identification of a classic nuclear localization signal at the N terminus that regulates the subcellular localization of Rbfox2 isoforms during diffe…

2016

Nuclear localization of the alternative splicing factor Rbfox2 is achieved by a C-terminal nuclear localization signal (NLS) which can be excluded from some Rbfox2 isoforms by alternative splicing. While this predicts nuclear and cytoplasmic localization, Rbfox2 is exclusively nuclear in some cell types. Here, we identify a second NLS in the N terminus of Rbfox2 isoform 1A that is not included in Rbfox2 isoform 1F. Rbfox2 1A isoforms lacking the C-terminal NLS are nuclear, whereas equivalent 1F isoforms are cytoplasmic. A shift in Rbfox2 expression toward cytoplasmic 1F isoforms occurs during epithelial to mesenchymal transition (EMT) and could be important in regulating the activity and fu…

0301 basic medicineGene isoformCytoplasmEpithelial-Mesenchymal TransitionNuclear Localization SignalsBiophysicsBiochemistryCell LineTransforming Growth Factor beta103 medical and health sciencesMiceMammary Glands AnimalProtein DomainsStructural BiologyCell Line TumorGeneticsNLSAnimalsProtein IsoformsAmino Acid SequenceMolecular BiologyCell NucleusChemistryAlternative splicingCell DifferentiationEpithelial CellsMouse Embryonic Stem CellsCell BiologySubcellular localizationMolecular biologyCell biologyAlternative Splicing030104 developmental biologyP19 cellCytoplasmRNA splicingRNA Splicing FactorsSequence AlignmentNuclear localization sequenceSignal TransductionFEBS letters
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Investigating fibrosis and inflammation in an ex vivo NASH murine model.

2020

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease, characterized by excess fat accumulation (steatosis). Nonalcoholic steatohepatitis (NASH) develops in 15–20% of NAFLD patients and frequently progresses to liver fibrosis and cirrhosis. We aimed to develop an ex vivo model of inflammation and fibrosis in steatotic murine precision-cut liver slices (PCLS). NASH was induced in C57Bl/6 mice on an amylin and choline-deficient l-amino acid-defined (CDAA) diet. PCLS were prepared from steatohepatitic (sPCLS) and control (cPCLS) livers and cultured for 48 h with LPS, TGFβ1, or elafibranor. Additionally, C57Bl/6 mice were placed on CDAA diet for 12 wk to receive elafibranor…

0301 basic medicineLipopolysaccharidesLiver CirrhosisMalePhysiologyHEPATOCYTESLiver diseaseMice0302 clinical medicineChalconesFibrosisNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseaseCells CulturedINSULIN-RESISTANCEGastroenterologyElafibranorTGF-BETALiver030211 gastroenterology & hepatologyCHOLINE-DEFICIENT DIETEXPRESSIONmedicine.medical_specialtyEARLY-ONSETIn Vitro TechniquesCollagen Type IProinflammatory cytokineTransforming Growth Factor beta103 medical and health sciencesIn vivoPhysiology (medical)Internal medicinemedicineAnimalsHEPATIC STEATOSISFATTY LIVER-DISEASEInflammationPRECISION-CUT LIVERHepatologybusiness.industrymedicine.diseaseLipid MetabolismDietMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyPROLIFERATOR-ACTIVATED RECEPTORSSteatosisPropionatesbusinessTranscriptomeEx vivoAmerican journal of physiology. Gastrointestinal and liver physiology
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Modulation of the TGF-β1-induced epithelial to mesenchymal transition (EMT) mediated by P1 and P2 purine receptors in MDCK cells

2017

Epithelial to mesenchymal transition (EMT) occurs during embryogenesis or under pathological conditions such as hypoxia, injury, chronic inflammation, or tissue fibrosis. In renal tubular epithelial cells (MDCK), TGF-β1 induces EMT by reducing or increasing epithelial or mesenchymal marker expression, respectively. In this study, we confirmed that the cAMP analogues, 8-CPT-cAMP or N6-Ph-cAMP, inhibited the TGF-β1-driven overexpression of the mesenchymal markers ZEB-1, Slug, Fibronectin, and α-SMA. Furthermore, we showed that A1, A2A, P2Y1, P2Y11, and P2X7 purine receptor agonists modulated the TGF-β1-induced EMT through the involvement of PKA and/or MAPK/ERK signaling. The stimulation o…

0301 basic medicineMAPK/ERK pathwayMadin Darby canine kidney cellEpithelial-Mesenchymal TransitionFibrosiCellTransforming growth factor β1InflammationStimulationBiologyEpithelial to mesenchymal transition; Fibrosis; Madin Darby canine kidney cells; P1/P2 purinergic receptors; Transforming growth factor β1; Molecular Biology; Cellular and Molecular Neuroscience; Cell BiologyTransforming Growth Factor beta103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDogsmedicineAnimalsEpithelial–mesenchymal transitionReceptorMolecular BiologyEpithelial to mesenchymal transitionP1/P2 purinergic receptorReceptors Purinergic P2Mesenchymal stem cellReceptors Purinergic P1Cell BiologyMadin Darby canine kidney cellsFibrosisCell biologyFibronectin030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisbiology.proteinP1/P2 purinergic receptorsOriginal ArticleTransforming growth factor β1medicine.symptomTransforming growth factor
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Urinary- and Plasma-Derived Exosomes Reveal a Distinct MicroRNA Signature Associated With Albuminuria in Hypertension.

2021

Urinary albumin excretion (UAE) is a marker of cardiovascular risk and renal damage in hypertension. MicroRNAs (miRNAs) packaged into exosomes function as paracrine effectors in cell communication and the kidney is not exempt. This study aimed to state an exosomal miRNA profile/signature associated to hypertension with increased UAE and the impact of profibrotic TGF-β1 (transforming growth factor β1) on exosomes miRNA release. Therefore, exosomes samples from patients with hypertension with/without UAE were isolated and characterized. Three individual and unique small RNA libraries from each subject were prepared (total plasma, urinary, and plasma-derived exosomes) for next-generation sequ…

0301 basic medicineMaleDown-Regulation030204 cardiovascular system & hematologyExosomesTransforming Growth Factor beta103 medical and health sciencesParacrine signalling0302 clinical medicinemicroRNAInternal MedicinemedicineAlbuminuriaHumansGene Regulatory NetworksKEGGCells CulturedAgedKidneybusiness.industryPodocytesReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingMiddle AgedMicrovesiclesMicroRNAs030104 developmental biologyReal-time polymerase chain reactionmedicine.anatomical_structureHypertensionAlbuminuriaCancer researchFemalemedicine.symptombusinessTransforming growth factorHypertension (Dallas, Tex. : 1979)
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Fasciola hepatica reinfection potentiates a mixed Th1/Th2/Th17/Treg response and correlates with the clinical phenotypes of anemia.

2016

Background: Fascioliasis is a severe zoonotic disease of worldwide extension caused by liver flukes. In human fascioliasis hyperendemic areas, reinfection and chronicity are the norm and anemia is the main sign. Herein, the profile of the Th1/Th2/Th17/Treg expression levels is analyzed after reinfection, correlating them with their corresponding hematological biomarkers of morbidity. Methodology/Principal findings: The experimental design reproduces the usual reinfection/chronicity conditions in human fascioliasis endemic areas and included Fasciola hepatica primo-infected Wistar rats (PI) and rats reinfected at 8 weeks (R8), and at 12 weeks (R12), and negative control rats. In a cross-sect…

0301 basic medicineMalePhysiologymedicine.medical_treatmentSnailslcsh:MedicineGene ExpressionImmune PhysiologyGene expressionMedicine and Health Scienceslcsh:ScienceImmune ResponseInnate Immune SystemMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionFOXP3hemic and immune systemsImmunosuppressionEBI3AnemiaForkhead Transcription FactorsHematologyThymusInterleukin-10Interleukin 10medicine.anatomical_structureHelminth InfectionsCytokinesResearch ArticleNeglected Tropical DiseasesFascioliasisImmunologychemical and pharmacologic phenomenaSpleenBiologyTransforming Growth Factor beta103 medical and health sciencesImmune systemTh2 CellsGeneticsParasitic DiseasesmedicineFasciola hepaticaAnimalsRats WistarCell ProliferationInterleukinslcsh:RBiology and Life SciencesMolecular DevelopmentFasciola hepaticaTh1 CellsTropical Diseasesbiology.organism_classificationRats030104 developmental biologyCross-Sectional StudiesImmune SystemImmunologyTh17 Cellslcsh:QSpleenDevelopmental Biology
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Alternative Splice Forms of CYLD Mediate Ubiquitination of SMAD7 to Prevent TGFB Signaling and Promote Colitis

2018

Background & Aims The CYLD lysine 63 deubiquitinase gene (CYLD) encodes tumor suppressor protein that is mutated in familial cylindromatosus, and variants have been associated with Crohn disease (CD). Splice forms of CYLD that lack exons 7 and 8 regulate transcription factors and functions of immune cells. We examined the expression of splice forms of CYLD in colon tissues from patients with CD and their effects in mice. Methods We performed immunohistochemical analyses of colon tissues from patients with untreated CD and patients without inflammatory bowel diseases (controls). We obtained mice that expressed splice forms of CYLD (sCYLD mice) without or with SMAD7 (sCYLD/SMAD7 mice) from tr…

0301 basic medicineTranscription FactorBiopsyInbred C57BLTransgenicImmune RegulationSettore MED/12MiceRandom Allocation0302 clinical medicineCrohn DiseaseReference ValuesNeedleIntestinal Mucosaintegumentary systemChemistryBiopsy NeedleGastroenterologyT helper cellFlow CytometryPost-translational ModificationImmunohistochemistryDeubiquitinating Enzyme CYLDCysteine Endopeptidasesmedicine.anatomical_structure030211 gastroenterology & hepatologyTumor necrosis factor alphaSignal TransductionGenetically modified mouseRegulatory T cellTransgeneMice TransgenicSmad7 ProteinTransforming Growth Factor beta103 medical and health sciencesImmune systemmedicineAnimalsHumansCytokine SignalingHepatologyAnimalHEK 293 cellsUbiquitinationMolecular biologyMice Inbred C57BLDisease Models Animal030104 developmental biologyDisease ModelsCytokine Signaling; Immune Regulation; Post-translational Modification; Transcription Factor; Biopsy Needle; Crohn Disease; Cysteine Endopeptidases; Deubiquitinating Enzyme CYLD; Disease Models Animal; Flow Cytometry; Immunohistochemistry; Intestinal Mucosa; Mice Inbred C57BL; Mice Transgenic; Random Allocation; Reference Values; Signal Transduction; Smad7 Protein; Transforming Growth Factor beta1; UbiquitinationTransforming growth factorGastroenterology
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Coexpression of TGF-β1 and IL-10 Enables Regulatory T Cells to Completely Suppress Airway Hyperreactivity

2008

Abstract In allergic airway disease, Treg may play an important role in the modulation of airway hyperreactivity (AHR) and inflammation. We therefore investigated the therapeutic potential of Treg in an Ag-dependent murine asthma model. We here describe that AHR can be completely suppressed by adoptive transfer of Treg overexpressing active TGF-β1. Using mice with impaired TGF-β signaling in T cells, we could demonstrate that TGF-β signaling in recipient effector T cells or transferred Treg themselves is not required for the protective effects on AHR. However, the expression of IL-10 by Treg was found to be essential for the suppression of AHR, since Treg overexpressing active TGF-β1 but de…

Adoptive cell transferTransgeneImmunologyGene ExpressionMice Transgenicchemical and pharmacologic phenomenaInflammationT-Lymphocytes RegulatoryTransforming Growth Factor beta1MiceRespiratory HypersensitivitymedicineAnimalsImmunology and AllergyAsthmaInflammationbusiness.industryEffectorhemic and immune systemsrespiratory systemmedicine.diseaseAdoptive TransferAirway hyperreactivityInterleukin-10respiratory tract diseasesDisease Models AnimalInterleukin 10Immunologymedicine.symptombusinessSignal TransductionTransforming growth factorThe Journal of Immunology
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