Search results for "Transforming growth factor"

showing 10 items of 294 documents

Steroid-growth factor interaction in human prostate cancer. 2. Effects of transforming growth factors on androgen metabolism of prostate cancer cells

1996

The ability of human prostate cancer cells to metabolize androgens was assessed through administration of physiological concentration (0.5-10 nM) of tritiated testosterone (T) as precursor and one-step analysis of both T degradation and products' formation by reverse-phase HPLC and on-line radioactive detection after either 24 h or 72 h incubation. Overall, different prostate cancer cells degraded T quite differently, favoring alternatively reductive or oxidative metabolic pathways. In particular, both LNCaP and DU145 cells retained high levels of unconverted T, with a limited production of androstenedione and its 17-keto derivatives and relatively high amounts of dihydrotestosterone (DHT) …

Malemedicine.medical_specialtymedicine.drug_classClinical BiochemistryBiologyurologic and male genital diseasesBiochemistrychemistry.chemical_compoundEndocrinologyDU145Transforming Growth Factor betaInternal medicineLNCaPTumor Cells CulturedmedicineHumansMolecular BiologyTestosteronePharmacologyAndrosteroneOrganic ChemistryProstatic NeoplasmsTransforming Growth Factor alphaAndrogenEndocrinologychemistryDihydrotestosteroneCancer cellAndrogensmedicine.drugTransforming growth factorSteroids
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Rac1 GTPase, a multifunctional player in the regulation of genotoxic stress response

2013

The Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the Ras-homologous (Rho) family of small GTPases, which transduce signals from the outside to the inside of a cell. Rac1 becomes activated upon ligand binding of a variety of receptors, including receptor tyrosine kinases and heterotrimeric G-protein-coupled receptors. After GTP loading by guanine exchange factors (GEFs), GTP-bound Rac1 engages numerous effector proteins, thereby eventually regulating cell motility and adhesion, cell cycle progression through G1, mitosis and meiosis, as well as cell death and metastasis.1 Besides, Rac1 adjusts cellular responses to genotoxic agents, such as UV light and alkylating agents, by r…

Malerac1 GTP-Binding Proteintopoisomerase IIAgingRHOADNA repairDNA damagep38 mitogen-activated protein kinasesApoptosisRAC1Editorials: Cell Cycle FeaturesDNA damage responseReceptor tyrosine kinasechemical carcinogenesisHistonesMiceTransforming Growth Factor betaRho GTPasesAnimalsMolecular BiologyTranscription factoranthracyclinesMice KnockoutbiologyKinaseNeuropeptidesConnective Tissue Growth FactorHMG-CoA reductase inhibitors (statins)Cell BiologyFibrosisgenotoxic stressActinsrac GTP-Binding ProteinsCell biologyOxidative Stressnormal tissue damageGene Expression RegulationLiverBiochemistryDoxorubicinGamma Raysbiology.proteinFemaleDNA DamageMutagensSignal TransductionDevelopmental BiologyCell Cycle
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Mitochondrial dynamics in type 2 diabetes: Pathophysiological implications

2017

Mitochondria play a key role in maintaining cellular metabolic homeostasis. These organelles have a high plasticity and are involved in dynamic processes such as mitochondrial fusion and fission, mitophagy and mitochondrial biogenesis. Type 2 diabetes is characterised by mitochondrial dysfunction, high production of reactive oxygen species (ROS) and low levels of ATP. Mitochondrial fusion is modulated by different proteins, including mitofusin-1 (MFN1), mitofusin-2 (MFN2) and optic atrophy (OPA-1), while fission is controlled by mitochondrial fission 1 (FIS1), dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF). PARKIN and (PTEN)-induced putative kinase 1 (PINK1) partici…

MiD51 mitochondrial dynamics proteins of 51 kDaΔΨm mitochondrial membrane potential0301 basic medicineMitochondrial fission factorClinical BiochemistryMitochondrial DegradationMFN2Review ArticleTXNIP thioredoxin interacting proteinMitochondrial DynamicsBiochemistryAdenosine TriphosphateGRP78 78 kDa glucose-regulated proteinMFF mitochondrial fission factorMFN2 mitofusin 2TRX2 thioredoxin 2Redox biologylcsh:QH301-705.5NF-κB nuclear factor kappa Blcsh:R5-920MitophagyType 2 diabetesDRP1 dynamin-related protein 1FIS1 fission protein 1BNIP3 BCL2/adenovirus E1B 19 kDa interacting protein 3MitochondriaOPA1 optic atrophy 1SIRT1/3 sirtuin 1/3Biochemistrymitochondrial fusionTGF-β1 transforming growth factor-β1Mitochondrial fissionOMM outer mitochondrial membranelcsh:Medicine (General)MiD49 mitochondrial dynamics proteins of 49Nox 4 NADPH oxidase-4IMM inner mitochondrial membraneFIS1ATF6 activating transcription factor 6PINK1mTOR mammalian target of rapamycinCHOP C/EBP homologous proteinBiologymdivi-1 mitochondrial division inhibitor-1Mitochondrial Proteins03 medical and health sciencesROS reactive oxygen speciessXBP1 spliced X-box binding protein 1UCP-1 uncoupling protein-1MFN1 mitofusin 1SOD superoxide dismutaseLC3 1 A/1B-light chain 3HumansPINK1 (PTEN)-induced putative kinase 1S3 15-OxospiramilactoneOrganic ChemistrymtDNA mitochondrial DNAAMPK AMP-activated protein kinase030104 developmental biologyDiabetes Mellitus Type 2Mitochondrial biogenesislcsh:Biology (General)Oxidative stressp38 MAPK p38 mitogen-activated protein kinasep62/SQSTM1 ubiquitin and sequestosome-1Reactive Oxygen SpeciesRedox Biology
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In murine 3T3 fibroblasts, different second messenger pathways resulting in the induction of NO synthase II (iNOS) converge in the activation of tran…

1996

Transcription factor NF-kappaB is essential for the induction of nitric oxide synthase (NOS) II (iNOS) by bacterial lipopolysaccharide in murine macrophages (Xie, Q. W., Kashiwabara, Y., and Nathan, C. (1994) J. Biol. Chem. 269, 4705-4708). In 3T3 fibroblasts, agents other than cytokines are efficacious inducers of NOS II expression. In addition to cytokines such as interferon-gamma or tumor necrosis factor-alpha, protein kinase C-stimulating agents such as tetradecanoylphorbol-13-acetate, or cyclic AMP-elevating agents such as forskolin and 8-bromo-cAMP markedly increased NOS II mRNA (measured by Sl nuclease and RNase protection analyses), NOS II protein (determined by Western blotting), a…

Molecular Sequence DataBiochemistrySecond Messenger SystemsDexamethasoneGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePyrrolidine dithiocarbamateTransforming Growth Factor betaAnimalsHumansAmino Acid SequenceRNA MessengerNuclear proteinProtein kinase AMolecular BiologyTranscription factorProtein Kinase CDNA PrimersForskolinbiologyBase SequenceNF-kappa BReceptor Protein-Tyrosine KinasesCell Biology3T3 CellsMolecular biologyCyclic AMP-Dependent Protein KinasesActinsNitric oxide synthasechemistryEnzyme InductionSecond messenger systembiology.proteinTumor necrosis factor alphaNitric Oxide SynthaseThe Journal of biological chemistry
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Bleomycin Exerts Ambivalent Antitumor Immune Effect by Triggering Both Immunogenic Cell Death and Proliferation of Regulatory T Cells

2013

International audience; Bleomycin (BLM) is an anticancer drug currently used for the treatment of testis cancer and Hodgkin lymphoma. This drug triggers cancer cell death via its capacity to generate radical oxygen species (ROS). However, the putative contribution of anticancer immune responses to the efficacy of BLM has not been evaluated. We make here the observation that BLM induces immunogenic cell death. In particular, BLM is able to induce ROS-mediated reticulum stress and autophagy, which result in the surface exposure of chaperones, including calreticulin and ERp57, and liberation of HMBG1 and ATP. BLM induces anti-tumor immunity which relies on calreticulin, CD8(+) T cells and inte…

MouseCancer TreatmentCD8-Positive T-LymphocytesT-Lymphocytes RegulatoryHematologic Cancers and Related DisordersMice0302 clinical medicineTransforming Growth Factor beta[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyCytotoxic T cellImmune Response0303 health sciencesMultidisciplinaryCell DeathbiologyQRFOXP3Animal ModelsHematology3. Good healthCell biologyOncology030220 oncology & carcinogenesisMedicine[SDV.IMM]Life Sciences [q-bio]/ImmunologyImmunogenic cell deathFemaleLymphomasOncology AgentsResearch ArticleTumor Immunologycongenital hereditary and neonatal diseases and abnormalitiesProgrammed cell death[SDV.IMM] Life Sciences [q-bio]/ImmunologyScienceImmunologyAntineoplastic Agentschemical and pharmacologic phenomenaBleomycin03 medical and health sciencesModel OrganismsImmune systemCell Line TumorAnimalsHumansBiologyCell Proliferation030304 developmental biologyHodgkin Lymphomaurogenital systemCell growthImmunitynutritional and metabolic diseasesImmunologic SubspecialtiesChemotherapy and Drug TreatmentImmunity InnateCancer cellbiology.proteinClinical ImmunologyCalreticulinPLoS ONE
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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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Cytokine Plasma Levels: Reliable Predictors for Radiation Pneumonitis?

2008

BackgroundRadiotherapy (RT) is the primary treatment modality for inoperable, locally advanced non-small-cell lung cancer (NSCLC), but even with highly conformal treatment planning, radiation pneumonitis (RP) remains the most serious, dose-limiting complication. Previous clinical reports proposed that cytokine plasma levels measured during RT allow to estimate the individual risk of patients to develop RP. The identification of such cytokine risk profiles would facilitate tailoring radiotherapy to maximize treatment efficacy and to minimize radiation toxicity. However, cytokines are produced not only in normal lung tissue after irradiation, but are also over-expressed in tumour cells of NSC…

OncologyPathologymedicine.medical_specialtyLung NeoplasmsSciencemedicine.medical_treatmentRespiratory Medicine/Lung CancerTransforming Growth Factor beta1Carcinoma Non-Small-Cell LungInternal medicineBiopsyBlood plasmamedicineCarcinomaHumansInterleukin 6Lung cancerOncology/Lung CancerPneumonitisMultidisciplinaryRadiotherapybiologymedicine.diagnostic_testInterleukin-6business.industryQRmedicine.diseaseRadiation PneumonitisRadiation therapyCytokineOncologybiology.proteinMedicineCytokinesbusinessBiomarkersResearch ArticlePLoS ONE
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Lung myofibroblasts are characterized by down-regulated cyclooxygenase-2 and its main metabolite, prostaglandin E2.

2013

Background: Prostaglandin E2 (PGE(2)), the main metabolite of cyclooxygenase (COX), is a well-known anti-fibrotic agent. Moreover, myofibroblasts expressing alpha-smooth muscle actin (alpha-SMA), fibroblast expansion and epithelial-mesenchymal transition (EMT) are critical to the pathogenesis of idiopathic pulmonary fibrosis (IPF). Our aim was to investigate the expression of COX-2 and PGE(2) in human lung myofibroblasts and establish whether fibroblast-myofibroblast transition (FMT) and EMT are associated with COX-2 and PGE(2) down-regulation. Methods: Fibroblasts obtained from IPF patients (n = 6) and patients undergoing spontaneous pneumothorax (control, n = 6) and alveolar epithelial ce…

PathologyPulmonologyMetaboliteImmunofluorescencelcsh:MedicineBiochemistrychemistry.chemical_compoundIdiopathic pulmonary fibrosisMolecular Cell BiologyPulmonary fibrosisProstaglandin E2Myofibroblastslcsh:ScienceLungCells CulturedFisiologia cel·lularMultidisciplinarybiologyFibrosi pulmonarrespiratory systemExtracellular Matrixmedicine.anatomical_structureCytokinesMedicinelipids (amino acids peptides and proteins)Immunohistochemical AnalysisMyofibroblastResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyEpithelial-Mesenchymal TransitionImmunologyInterstitial Lung DiseasesDinoprostonePulmonary fibrosisTransforming Growth Factor beta1ImmunofluorescènciaGrowth FactorsCell Line TumormedicineHumansEpithelial–mesenchymal transitionFibroblastBiologyCell Proliferationlcsh:RProteinsEpithelial Cellsmedicine.diseaseActinsIdiopathic Pulmonary Fibrosisrespiratory tract diseasesGene Expression RegulationchemistryCyclooxygenase 2Immune SystemCase-Control StudiesImmunologic Techniquesbiology.proteinCancer researchClinical Immunologylcsh:QCyclooxygenaseBiomarkersPLoS ONE
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Involvement of distal airways in a chronic model of experimental asthma.

2005

Summary Background Bronchial asthma is characterized by chronic airway inflammation and airway remodelling which occurs in both proximal and distal airways. These changes are associated with development of airway hyper-responsiveness and airflow limitation. Objective This study was aimed to analyse whether chronic inhalative allergen challenges in mice lead to morphological and physiological changes comparable with this phenotype. Methods For this purpose, BALB/c mice were systemically sensitized to ovalbumin (OVA) followed by aerosol allergen challenges on 2 consecutive days per week for 12 weeks. Results In chronically challenged mice, tissue inflammation in proximal as well as distal air…

Pathologymedicine.medical_specialtyAllergyOvalbuminImmunologyInflammationBronchiMiceTransforming Growth Factor betaAdministration InhalationmedicineImmunology and AllergyAnimalsRespiratory systemAsthmaMice Inbred BALB CMucous MembraneInhalationbusiness.industryRespiratory diseaserespiratory systemAllergensmedicine.diseaseAsthmarespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureImmunologyChronic DiseaseDisease ProgressionCytokinesFemalemedicine.symptomBronchial HyperreactivityAirwaybusinessBronchoalveolar Lavage FluidRespiratory tractClinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
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SPARC oppositely regulates inflammation and fibrosis in bleomycin-induced lung damage.

2011

Fibrosis results from inflammatory tissue damage and impaired regeneration. In the context of bleomycin-induced pulmonary fibrosis, we demonstrated that the matricellular protein termed secreted protein acidic and rich in cysteine (SPARC) distinctly regulates inflammation and collagen deposition, depending on its cellular origin. Reciprocal Sparc(-/-) and wild-type (WT) bone marrow chimeras revealed that SPARC expression in host fibroblasts is required and sufficient to induce collagen fibrosis in a proper inflammatory environment. Accordingly, Sparc(-/-) >WT chimeras showed exacerbated inflammation and fibrosis due to the inability of Sparc(-/-) macrophages to down-regulate tumor necrosis …

Pathologymedicine.medical_specialtyAnimals; Bleomycin; Bone Marrow Cells; Chimera; Collagen; Down-Regulation; Fibroblasts; Leukocytes; Macrophages; Mice; Mice Inbred BALB C; Osteonectin; Pneumonia; Pulmonary Fibrosis; Transforming Growth Factor beta; Tumor Necrosis Factor-alphaPulmonary FibrosisDown-RegulationInflammationBone Marrow CellsBiologyPathology and Forensic MedicineMiceFibrosisTumor necrosis factor productionTransforming Growth Factor betaPulmonary fibrosismedicineLeukocytesAnimalsOsteonectinInbred BALB CChimeraTumor Necrosis Factor-alphaMacrophagesMatricellular proteinRegular ArticleSPARCTransforming growth factor betaPneumoniaFibroblastsBLEOMYCINmedicine.diseaseSPARC; BLEOMYCIN; LUNG DAMAGELUNG DAMAGECancer researchbiology.proteinTumor necrosis factor alphaCollagenmedicine.symptomOsteonectin
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