Search results for "Transforming Growth Factor beta1"

showing 10 items of 72 documents

Poly(γ-Glutamic Acid) as an Exogenous Promoter of Chondrogenic Differentiation of Human Mesenchymal Stem/Stromal Cells

2015

Cartilage damage and/or aging effects can cause constant pain, which limits the patient's quality of life. Although different strategies have been proposed to enhance the limited regenerative capacity of cartilage tissue, the full production of native and functional cartilaginous extracellular matrix (ECM) has not yet been achieved. Poly(γ-glutamic acid) (γ-PGA), a naturally occurring polyamino acid, biodegradable into glutamate residues, has been explored for tissue regeneration. In this work, γ-PGA's ability to support the production of cartilaginous ECM by human bone marrow mesenchymal stem/stromal cells (MSCs) and nasal chondrocytes (NCs) was investigated. MSC and NC pellets were cultur…

Stromal cellBiomedical EngineeringType II collagenCell Culture TechniquesBioengineeringBiochemistryBiomaterialsExtracellular matrixTransforming Growth Factor beta1ChondrocytesNasal CartilagesmedicineHumansAggrecansAggrecanCells CulturedGlycosaminoglycansExtracellular Matrix ProteinsChemistryCartilageMesenchymal stem cellMesenchymal Stem CellsSOX9 Transcription FactorOriginal ArticlesChondrogenesisMolecular biologyCulture Mediamedicine.anatomical_structureBiochemistryPolyglutamic AcidCulture Media ConditionedCalciumCollagenStromal CellsChondrogenesisType I collagen
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Chronic myeloid leukemia-derived exosomes promote tumor growth through an autocrine mechanism.

2014

Background Chronic myeloid leukemia (CML) is a clonal hematopoietic stem cell disorder in which leukemic cells display a reciprocal t(9:22) chromosomal translocation that results in the formation of the chimeric BCR-ABL oncoprotein, with a constitutive tyrosine kinase activity. Consequently, BCR-ABL causes increased proliferation, inhibition of apoptosis, and altered adhesion of leukemic blasts to the bone marrow (BM) microenvironment. It has been well documented that cancer cells can generate their own signals in order to sustain their growth and survival, and recent studies have revealed the role of cancer-derived exosomes in activating signal transduction pathways involved in cancer cell…

SurvivinMice NudeMice SCIDBiologyAutocrine mechanismsExosomesBiochemistryExosomeInhibitor of Apoptosis ProteinsTransforming Growth Factor beta1Micehemic and lymphatic diseasesCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveTGF-β1medicineAnimalsHumansAutocrine signallingMolecular BiologyCell ProliferationTumor microenvironmentCell growthResearchChronic myeloid leukemiaMyeloid leukemiaCell Biologymedicine.diseaseMicrovesiclesCML exosomesCell biologyNeoplasm ProteinsLeukemiaAutocrine CommunicationCancer cellAnti-apoptotic pathwaysApoptosis Regulatory ProteinsSignal TransductionCell communication and signaling : CCS
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Vitamin A deficiency alters rat lung alveolar basement membrane: reversibility by retinoic acid.

2010

Vitamin A is essential for lung development and pulmonary cell differentiation and its deficiency results in alterations of lung structure and function. Basement membranes (BMs) are also involved in those processes, and retinoic acid, the main biologically active form of vitamin A, influences the expression of extracellular matrix macromolecules. Therefore, we have analyzed the ultrastructure and collagen content of lung alveolar BM in growing rats deficient in vitamin A and the recovering effect of all-trans retinoic acid. Male weanling pups were fed a retinol-adequate or -deficient diet until they were 60 days old. A group of vitamin A-deficient pups were recovered by daily intraperitonea…

VitaminCollagen Type IVMalemedicine.medical_specialtymedicine.drug_classEndocrinology Diabetes and MetabolismClinical BiochemistryRetinoic acidTretinoinBiochemistryBasement MembraneCollagen Type ITransforming Growth Factor beta1chemistry.chemical_compoundInternal medicineMalondialdehydemedicineAnimalsRetinoidRNA MessengerRats WistarMolecular BiologyLungPeroxidaseBasement membraneNutrition and DieteticsLungbiologyTumor Necrosis Factor-alphaVitamin A DeficiencyInterleukinsRetinolmedicine.diseaseImmunohistochemistryRatsVitamin A deficiencyPulmonary AlveoliOxidative StressProtein SubunitsEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationMyeloperoxidasebiology.proteinThe Journal of nutritional biochemistry
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Inhibition of HSP27 blocks fibrosis development and EMT features by promoting Snail degradation

2013

Idiopathic pulmonary fibrosis (IPF) is a devastating disease characterized by myofibroblast proliferation. Transition of epithelial/mesothelial cells into myofibroblasts [epithelial-to-mesenchymal transition (EMT)] occurs under the influence of transforming growth factor (TGF)-β1, with Snail being a major transcription factor. We study here the role of the heat-shock protein HSP27 in fibrogenesis and EMT. In vitro, we have up- and down-modulated HSP27 expression in mesothelial and epithelial cell lines and studied the expression of different EMT markers induced by TGF-β1. In vivo, we inhibited HSP27 with the antisense oligonucleotide OGX-427 (in phase II clinical trials as anticancer agent)…

endocrine systemPathologymedicine.medical_specialtyEpithelial-Mesenchymal Transitionanimal structuresSnailsHSP27 Heat-Shock ProteinsBiologyBiochemistryCell LineRats Sprague-DawleyTransforming Growth Factor beta103 medical and health sciencesIdiopathic pulmonary fibrosis0302 clinical medicineIn vivoFibrosisPulmonary fibrosisGeneticsmedicineAnimalsHumansEpithelial–mesenchymal transitionMolecular Biology030304 developmental biology0303 health sciencesGene knockdownEpithelial CellsOligonucleotides AntisenseThionucleotidesCadherinsmedicine.diseaseFibrosisRats3. Good health030220 oncology & carcinogenesisembryonic structuresCancer researchMyofibroblastTranscription FactorsBiotechnologyTransforming growth factorThe FASEB Journal
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Gene expression in TGFbeta-induced epithelial cell differentiation in a three-dimensional intestinal epithelial cell differentiation model

2006

Abstract Background The TGFβ1-induced signal transduction processes involved in growth and differentiation are only partly known. The three-dimensional epithelial differentiation model, in which T84 epithelial cells are induced to differentiate either with TGFβ1 or IMR-90 mesenchymal cell-secreted soluble factors, is previously shown to model epithelial cell differentiation seen in intestine. That model has not been used for large scale gene expression studies, such as microarray method. Therefore the gene expression changes were studied in undifferentiated and differentiated three-dimensional T84 cultures with cDNA microarray method in order to study the molecular changes and find new play…

geenien ilmeneminenlcsh:QH426-470ColonCellular differentiationlcsh:BiotechnologyCell Culture TechniquesBiologyMesodermTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineLääketieteen bioteknologia - Medical biotechnologyCell Line Tumorlcsh:TP248.13-248.65Gene expressionGeneticsHumansIntestinal epithelial cell differentiationTGF-betageeniekspressioIntestinal MucosaOligonucleotide Array Sequence Analysis030304 developmental biologyEpithelial cell differentiationRegulation of gene expression0303 health sciencesTGB-betaepithelial cellMesenchymal stem cellCell DifferentiationEpithelial CellsdifferentiationFibroblastsepiteelisoluMolecular biologyCell biologylcsh:GeneticsGene Expression RegulationerilaistuminenCell culture030220 oncology & carcinogenesisSignal transductionmicroarraygeenilastuSignal TransductionResearch ArticleBiotechnology
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Regulatory cytokine gene polymorphisms and risk of colorectal carcinoma.

2006

It is well established that cancer arises in chronically inflamed tissue, and this is particularly notable in the gastrointestinal tract. Classic examples include Helicobacter pylori-associated gastric cancer, hepatocellular carcinoma, and inflammatory bowel disease-associated colorectal cancer. Growing evidence suggests that these associations might be not casual findings. Focusing on individual cytokines has generated evidence that anti-inflammatory cytokine interleukin (IL)-10 and transforming growth factor-beta1 (TGF-beta1) may have a complex role in gastrointestinal carcinogenesis. As an example, IL-10-deficient mice develop severe atrophic gastritis and a chronic enterocolitis, develo…

gene polymorphismsMaleRiskProlineColorectal cancerAtrophic gastritisil-10colorectal cancerMouse model of colorectal and intestinal cancerBiologymedicine.disease_causePolymorphism Single NucleotideGeneral Biochemistry Genetics and Molecular BiologyMetastasisTransforming Growth Factor beta1colorectal cancercytokine genepolymorphismsHistory and Philosophy of ScienceGene FrequencyLeucineGenotypemedicineHumansGenetic Predisposition to DiseaseAllelesGeneral Neurosciencetgf-β1CarcinomaCancermedicine.diseaseInterleukin-10Amino Acid SubstitutionItalyTumor progressionCase-Control StudiesImmunologycolorectal cancer; gene polymorphisms; il-10; tgf-β1FemaleCarcinogenesisColorectal NeoplasmsAnnals of the New York Academy of Sciences
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Analysis of molecular mechanisms and anti-tumoural effects of zoledronic acid in breast cancer cells

2012

Zoledronic acid (ZOL) is the most potent nitrogen-containing bisphosphonate (N-BPs) that strongly binds to bone mineral and acts as a powerful inhibitor of bone resorption, already clinically available for the treatment of patients with osteolytic metastases. Recent data also suggest that ZOL, used in breast cancer, may provide more than just supportive care modifying the course of the disease, though the possible molecular mechanism of action is still unclear. As breast cancer is one of the primary tumours with high propensity to metastasize to the bone, we investigated, for the first time, differential gene expression profile on Michigan Cancer Foundation-7 (MCF-7) breast cancer cells tre…

medicine.medical_specialtyAngiogenesismedicine.medical_treatmentBlotting WesternAngiogenesis InhibitorsAntineoplastic AgentsBreast NeoplasmsBiologyReal-Time Polymerase Chain ReactionZoledronic AcidZOL FN1 TGF-b1 THBS-1 invasion breast cancerBone resorptionThrombospondin 1Transforming Growth Factor beta1breast cancerBreast cancerTGF-β1Internal medicineThrombospondin 1medicineHumansBone ResorptionCell ProliferationMatrigelDiphosphonatesFN1Gene Expression ProfilingImidazolesCancerOriginal ArticlesCell BiologyZOLBisphosphonateMicroarray Analysisinvasionmedicine.diseaseFibronectinsUp-RegulationGene Expression Regulation NeoplasticEndocrinologyZoledronic acidTHBS-1MCF-7 CellsCancer researchMolecular MedicineFemalemedicine.drug
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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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Estradiol Stimulates Vasodilatory and Metabolic Pathways in Cultured Human Endothelial Cells

2009

Vascular effects of estradiol are being investigated because there are controversies among clinical and experimental studies. DNA microarrays were used to investigate global gene expression patterns in cultured human umbilical vein endothelial cells (HUVEC) exposed to 1 nmol/L estradiol for 24 hours. When compared to control, 187 genes were identified as differentially expressed with 1.9-fold change threshold. Supervised principal component analysis and hierarchical cluster analysis revealed the differences between control and estradiol-treated samples. Physiological concentrations of estradiol are sufficient to elicit significant changes in HUVEC gene expression. Notch signaling, actin cyt…

medicine.medical_specialtyUmbilical Veinsmedicine.drug_classScienceEstrogen receptorBiologyAmidohydrolasesTransforming Growth Factor beta1chemistry.chemical_compoundInternal medicinemedicineCluster AnalysisEstrogen Receptor betaHumansEstrogen receptor betaCell Biology/Gene ExpressionCells CulturedOligonucleotide Array Sequence AnalysisRegulation of gene expressionPrincipal Component AnalysisMultidisciplinaryEstradiolPhysiology/EndocrinologyReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingQPhysiology/Cardiovascular Physiology and CirculationREstrogen Receptor alphaEndothelial CellsReproducibility of ResultsActin cytoskeletonVasodilationEndocrinologychemistryGene Expression RegulationEstrogenCyclooxygenase 1MedicineSignal transductionAsymmetric dimethylarginineEstrogen receptor alphahormones hormone substitutes and hormone antagonistsMetabolic Networks and PathwaysResearch ArticleSignal TransductionPLoS ONE
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