Search results for "TGF-Β"

showing 10 items of 26 documents

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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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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Bi-allelic LoF NRROS Variants Impairing Active TGF-β1 Delivery Cause a Severe Infantile-Onset Neurodegenerative Condition with Intracranial Calcifica…

2020

Negative regulator of reactive oxygen species (NRROS) is a leucine-rich repeat-containing protein that uniquely associates with latent transforming growth factor beta-1 (TGF- β1) and anchors it on the cell surface; this anchoring is required for activation of TGF-β1 in macrophages and microglia. We report six individuals from four families with bi-allelic variants in NRROS. All affected individuals had neurodegenerative disease with refractory epilepsy, developmental regression, and reduced white matter volume with delayed myelination. The clinical course in affected individuals began with normal development or mild developmental delay, and the onset of seizures occurred within the first ye…

Male0301 basic medicineInflammationBiologyintracranial calcificationneuroinflammationTransforming Growth Factor beta103 medical and health sciences0302 clinical medicineReportTGF-β1NRROSGeneticsmedicineHumansAllelesGenetics (clinical)NeuroinflammationBrain DiseasesMicrogliaMacrophagesNeurodegenerationneurodegenerationCalcinosisGenetic VariationInfantNeurodegenerative Diseasesmedicine.diseaseNFKB1Latent TGF-beta binding proteinHEK293 Cells030104 developmental biologymedicine.anatomical_structureLatent TGF-beta Binding ProteinsImmunologyKnockout mouseFemaleMicrogliamutationmedicine.symptomDevelopmental regression030217 neurology & neurosurgeryThe American Journal of Human Genetics
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GARP: A Key Target to Evaluate Tumor Immunosuppressive Microenvironment

2021

Simple Summary Tumors are not only composed of cancer cells but also of various infiltrating cells constituting the tumor microenvironment (TME); all these cells produce growth factors which contribute to tumor progression and invasiveness. Among them, transforming growth factor-β1 (TGF-β1) has been shown to be a potent immunosuppressive cytokine favoring cell proliferation and invasion and to be associated with resistance to anticancer treatments. Glycoprotein-A repetition predominant (GARP) plays a critical role in the activation of TGF-β1 and has been shown to be expressed at the membrane of cancer cells and also of regulatory T cells and platelets in the TME. An increased GARP expressio…

TGF-βTumor microenvironmentimmunosuppressionGeneral Immunology and MicrobiologyQH301-705.5CancerReviewBiologymedicine.diseaseGeneral Biochemistry Genetics and Molecular BiologyBiomarker (cell)Docking (dog)Immune systemGARPCancer researchmedicinecancerbiomarkerBiology (General)General Agricultural and Biological SciencesReceptorFunction (biology)Transforming growth factorBiology
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The Endothelial Transcription Factor ERG Mediates a Differential Role in the Aneurysmatic Ascending Aorta with Bicuspid or Tricuspid Aorta Valve: A P…

2022

The pathobiology of ascending aorta aneurysms (AAA) onset and progression is not well understood and only partially characterized. AAA are also complicated in case of bicuspid aorta valve (BAV) anatomy. There is emerging evidence about the crucial role of endothelium-related pathways, which show in AAA an altered expression and function. Here, we examined the involvement of ERG-related pathways in the differential progression of disease in aortic tissues from patients having a BAV or tricuspid aorta valve (TAV) with or without AAA. Our findings identified ERG as a novel endothelial-specific regulator of TGF-β-SMAD, Notch, and NO pathways, by modulating a differential fibrotic or calcified A…

NotchHeart Valve DiseasesCatalysisInorganic ChemistryBicuspid Aortic Valve DiseaseTranscriptional Regulator ERGascending aorta aneurysm; bicuspid aorta valve; tricuspid aorta valve; ERG transcriptional factor pathway; TGF-β-SMAD; Notch; NO pathways modulationTransforming Growth Factor betaSettore MED/05 - Patologia ClinicaHumansTGF-β-SMADEndotheliumPhysical and Theoretical ChemistryMolecular BiologySpectroscopyAortabicuspid aorta valveOrganic ChemistryERG transcriptional factor pathwayGeneral Medicineascending aorta aneurysmComputer Science ApplicationsSettore MED/23Aortic Valvetricuspid aorta valveNO pathways modulationBiomarkersTranscription FactorsInternational Journal of Molecular Sciences; Volume 23; Issue 18; Pages: 10848
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Myostatin and related proteins on the control of skeletal muscle mass and capillary density

2013

Skeletal muscle wasting is a feature of many pathological conditions such as muscular dystrophies, cancer and diabetes. Human ageing also results in the progressive loss of muscle mass and strength, a condition known as sarcopenia (or myopenia). Therefore, interventions that can reverse or slow down muscle loss are highly desirable. The TGF-β member myostatin is a well-known inhibitor of skeletal muscle growth, but it may also, if deleted, decrease muscle oxidative capacity. We have used the activin receptor 2B (ActR2B) fused to the Fc region of immunoglobulin G (ActR2B-Fc) as a trap to sequester myostatin and inhibit its activity. We sought to evaluate possible differences between doses an…

TGF-βactivin receptor 2Bmyostatinliikakasvulihaksetproteiinitskeletal musclehypertrophy
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Treatment with soluble activin type IIB-receptor improves bone mass and strength in a mouse model of Duchenne muscular dystrophy

2017

Background: Inhibition of activin/myostatin pathway has emerged as a novel approach to increase muscle mass and bone strength. Duchenne muscular dystrophy (DMD) is a neuromuscular disorder that leads to progressive muscle degeneration and also high incidence of fractures. The aim of our study was to test whether inhibition of activin receptor IIB ligands with or without exercise could improve bone strength in the mdx mouse model for DMD. Methods: Thirty-two mdx mice were divided to running and non-running groups and to receive either PBS control or soluble activin type IIB-receptor (ActRIIB-Fc) once weekly for 7 weeks. Results: Treatment of mdx mice with ActRIIB-Fc resulted in significantly…

bone-muscle interactionsOXIDATIVE CAPACITYMDX MICEbone μCTexerciseBLOCKINGBone mu CTEXERCISEPREVENTS3126 Surgery anesthesiology intensive care radiologyMYOSTATINBone-muscle interactionsanimal modelsAnimal modelsDEFICIENCYTGF-βsDENSITY3121 General medicine internal medicine and other clinical medicineMUSCLE PROTEIN-SYNTHESISOrthopedics and Sports MedicineTGF-beta sMETAANALYSIS
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Mutations in SKI in Shprintzen-Goldberg syndrome lead to attenuated TGF-β responses through SKI stabilization.

2020

ABSTRACTShprintzen-Goldberg syndrome (SGS) is a multisystemic connective tissue disorder, with considerable clinical overlap with Marfan and Loeys-Dietz syndromes. These syndromes have commonly been associated with enhanced TGF-β signaling. In SGS patients, heterozygous point mutations have been mapped to the transcriptional corepressor SKI, which is a negative regulator of TGF-β signaling that is rapidly degraded upon ligand stimulation. The molecular consequences of these mutations, however, are not understood. Here we use a combination of structural biology, genome editing and biochemistry to show that SGS mutations in SKI abolish its binding to phosphorylated SMAD2 and SMAD3. This resul…

0301 basic medicineMaleSMADmedicine.disease_causeMarfan SyndromeActivin0302 clinical medicineGenome editingTransforming Growth Factor betaGene expressionBiology (General)MutationShprintzen-Goldberg syndromeGeneral NeuroscienceQRShprintzen–Goldberg syndromeGeneral MedicineLigand (biochemistry)Chromosomes and Gene ExpressionCell biologyDNA-Binding ProteinsMedicinePhosphorylationFemaleSignal TransductionResearch ArticleHumanTGF-βQH301-705.5ScienceBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCraniosynostosesstomatognathic systemBiochemistry and Chemical BiologyProto-Oncogene ProteinsmedicineHumansGeneral Immunology and MicrobiologyPoint mutationmedicine.diseaseSKIArachnodactyly030104 developmental biologyStructural biologyMutation030217 neurology & neurosurgerySMADTransforming growth factoreLife
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The role of the fibronectin synergy site in skin wound healing

2022

Upon skin barrier disruption, complex cellular and molecular events are activated to repair the damage and restore skin integrity. In adulthood, the outcome of this process can result in scarring and fibrosis, whereas complete tissue regeneration is observed in fetal wounds and wounds in lower vertebrates and invertebrates .Although there is abundant literature about the factors and mechanisms that determine the endpoint of either scarring/fibrosis or regeneration after tissue injury, the process is still poorly understood. After cutaneous injury, fibronectin (FN) is instantly released and deposited by cells, and represents a major ECM component in all stages of the wound healing process. F…

TGF-β1myofibroblastsUNESCO::CIENCIAS DE LA VIDAsynergy sitewound healingα5β1 integrinfibronecin
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TNFSF14 (LIGHT) Exhibits Inflammatory Activities in Lung Fibroblasts Complementary to IL-13 and TGF-β

2018

The cytokine TNFSF14 [homologous to Lymphotoxin, exhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEM, a receptor expressed on T lymphocytes (LIGHT)] has been shown in mouse models to be important for development of lung tissue remodeling that is characteristic of asthma, idiopathic pulmonary fibrosis (IPF), and systemic sclerosis (SSc). However, its cellular targets are not fully delineated. In the present report, we show that LTβR and HVEM, the receptors for LIGHT, are constitutively expressed in primary human lung fibroblasts (HLFs). We asked whether LIGHT could promote inflammatory and remodeling-relevant activity in HLFs and how this was similar to, or…

0301 basic medicinelcsh:Immunologic diseases. AllergyTGF-βChemokineTumor Necrosis Factor Ligand Superfamily Member 14medicine.medical_treatmentImmunologyGene ExpressionInflammationProinflammatory cytokineCell Line03 medical and health sciences0302 clinical medicineTransforming Growth Factor betamedicineImmunology and AllergyHumansLungCells CulturedOriginal ResearchCell ProliferationInterleukin-13biologyChemistrylung fibroblastsasthmaFibroblasts3. Good healtha receptor expressed on T lymphocytes030104 developmental biologyCytokineLymphotoxinCXCL5030220 oncology & carcinogenesisIL-13Interleukin 13biology.proteinCancer researchCytokinesexhibits Inducible expression and competes with HSV Glycoprotein D for binding to HVEMmedicine.symptomhomologous to LymphotoxinInflammation Mediatorslcsh:RC581-607MyofibroblastBiomarkersFrontiers in Immunology
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