Search results for " Transforming Growth Factor Beta"

showing 4 items of 34 documents

TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
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Smad7 controls resistance of colitogenic T cells to regulatory T cell-mediated suppression.

2008

Background & Aims Foxp3-expressing regulatory T cells (Tregs) play a key role in the maintenance of the gut immune homeostasis, and an intact transforming growth factor (TGF)-β signaling is required for their function. In inflammatory bowel disease (IBD), the TGF-β signaling is impaired because of high expression of the inhibitory molecule Smad7. Although no intrinsic defects in Tregs function have been shown in IBD, it is still unknown whether colitogenic T cells are susceptible to Treg-mediated suppression. In this study, we have investigated whether IBD mucosal CD4+ T cells are resistant to Tregs and whether Smad7 is involved in this process. Methods IBD lamina propria mononuclear cells …

antisense oligonucleotideCD4-Positive T-LymphocytesAdoptive cell transferT-Lymphocytesanimal cellCell CommunicationInbred C57BLT-Lymphocytes RegulatoryTransgenicMiceregulatory T lymphocyteCrohn DiseaseTransforming Growth Factor betamononuclear cellRAG1 proteinIntestinal MucosaenteritisCells CulturedMice KnockoutSettore MED/12 - GastroenterologiaCulturedintegumentary systemmedicine.diagnostic_testarticleGastroenterologyInterleukinhemic and immune systemsT helper cellColitisRegulatoryUp-Regulationmedicine.anatomical_structurepriority journalgamma interferonSignal TransductionRegulatory T cellColonCellsKnockoutanimal experimentinterleukin 6chemical and pharmacologic phenomenaMice TransgenicBiologyinterleukin 2Recombination-activating geneFlow cytometryProinflammatory cytokineSmad7 ProteinmedicineAnimalsHumanscontrolled studyhumanlamina propriamouseCell ProliferationHomeodomain ProteinsCD4+ T lymphocytenonhumanHepatologyAnimalflow cytometryhuman cellanimal cell culturetransgenic mouseMice Inbred C57BLDisease Models Animalantisense oligonucleotide; gamma interferon; interleukin 17; interleukin 2; interleukin 6; RAG1 protein; Smad7 protein; animal cell; animal cell culture; animal experiment; article; CD4+ T lymphocyte; cell proliferation; colitis; controlled study; enteritis; flow cytometry; human; human cell; knockout mouse; lamina propria; mononuclear cell; mouse; nonhuman; priority journal; regulatory T lymphocyte; transgenic mouse; Animals; CD4-Positive T-Lymphocytes; Cell Communication; Cell Proliferation; Cells Cultured; Colitis; Colon; Crohn Disease; Disease Models Animal; Homeodomain Proteins; Humans; Intestinal Mucosa; Mice; Mice Inbred C57BL; Mice Knockout; Mice Transgenic; Signal Transduction; Smad7 Protein; T-Lymphocytes Regulatory; Transforming Growth Factor beta; Up-RegulationDisease ModelsImmunologyinterleukin 17knockout mouseTransforming growth factorGastroenterology
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Developmental and tumoral vascularization is regulated by G protein-coupled receptor kinase 2

2012

Tumor vessel dysfunction is a pivotal event in cancer progression. Using an in vivo neovascularization model, we identified G protein–coupled receptor kinase 2 (GRK2) as a key angiogenesis regulator. An impaired angiogenic response involving immature vessels was observed in mice hemizygous for Grk2 or in animals with endothelium-specific Grk2 silencing. ECs isolated from these animals displayed intrinsic alterations in migration, TGF-β signaling, and formation of tubular networks. Remarkably, an altered pattern of vessel growth and maturation was detected in postnatal retinas from endothelium-specific Grk2 knockout animals. Mouse embryos with systemic or endothelium-selective Grk2 ablation …

medicine.medical_specialtyG-Protein-Coupled Receptor Kinase 2Angiogenic SwitchAngiogenesisMedicinaActivin Receptors Type IIMelanoma ExperimentalReceptor Transforming Growth Factor-beta Type INeovascularization PhysiologicProtein Serine-Threonine KinasesBiologyMural cellGrk2Transforming Growth Factor beta1NeovascularizationMiceDownregulation and upregulationCell MovementPregnancyInternal medicinemedicineAnimalsHumansCell ProliferationHemizygoteMice KnockoutG protein-coupled receptor kinaseTumorNeovascularization PathologicEndothelial CellsRetinal VesselsG proteinGeneral MedicineCell biologyEndocrinologymedicine.anatomical_structurecardiovascular systemFemalePericyteSignal transductionmedicine.symptomActivin Receptors Type IReceptors Transforming Growth Factor betaSignal TransductionResearch Article
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Progressive pulmonary fibrosis is mediated by TGF-β isoform 1 but not TGF-β3

2007

Tissue repair is a well-orchestrated biological process involving numerous soluble mediators, and an imbalance between these factors may result in impaired repair and fibrosis. Transforming growth factor (TGF)-beta is a key profibrotic element in this process and it is thought that its three isoforms act in a similar way. Here, we report that TGF-beta3 administered to rat lungs using transient overexpression initiates profibrotic effects similar to those elicited by TGF-beta1, but causes less severe and progressive changes. The data suggest that TGF-beta3 does not lead to inhibition of matrix degradation in the same way as TGF-beta1, resulting in non-fibrotic tissue repair. Further, TGF-bet…

medicine.medical_specialtyPulmonary FibrosisSMADBiologyBiochemistryArticleCell LineRats Sprague-DawleyTransforming Growth Factor beta1Extracellular matrixTransforming Growth Factor beta3Downregulation and upregulationFibrosisInternal medicinePulmonary fibrosismedicineAnimalsLungCell Biologymedicine.diseaseRatsCTGFEndocrinologyCancer researchFemaleWound healingReceptors Transforming Growth Factor betaTransforming growth factorThe International Journal of Biochemistry & Cell Biology
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