Search results for " Transcription factor"

showing 10 items of 656 documents

Expression of angiogenic regulators, VEGF and leptin, is regulated by the EGF/PI3K/STAT3 pathway in colorectal cancer cells.

2009

Both leptin and vascular endothelial growth factor (VEGF) are growth and angiogenic cytokines that are upregulated in different types of cancer and have been implicated in neoplastic progression. Here we investigated the molecular mechanism by which leptin and VEGF expression are regulated in colon cancer by epidermal growth factor (EGF). In colon cancer cell line HT-29, EGF induced the binding of signal transducer and activator transcription 3 (STAT3) to STAT3 consensus motifs within the VEGF and leptin promoters and stimulated leptin and VEGF mRNA and protein synthesis. All these EGF effects were significantly blocked when HT-29 cells were treated with an inhibitor of the phosphoinositide…

LeptinSTAT3 Transcription FactorVascular Endothelial Growth Factor ASmall interfering RNAPhysiologyColorectal cancerClinical BiochemistryNeovascularization PhysiologicEGF/PI3K/STAT3colorectal cancerchemistry.chemical_compoundPhosphatidylinositol 3-KinasesEpidermal growth factormedicineHumansLY294002Gene SilencingRNA MessengerSTAT3Promoter Regions GeneticPI3K/AKT/mTOR pathwayCell NucleusbiologyEpidermal Growth FactorChemistryLeptinangiogenic regulators VEGF leptinCell Biologymedicine.diseaseUp-RegulationVascular endothelial growth factorGene Expression Regulation NeoplasticCancer researchbiology.proteinColorectal NeoplasmsHT29 Cellshormones hormone substitutes and hormone antagonistsProtein Binding
researchProduct

Fluticasone furoate maintains epithelial homeostasis via leptin/leptin receptor pathway in nasal cells

2014

Leptin is involved in the lung epithelial homeostasis. Its role in the nasal tract is largely unknown. Allergic rhinitis (AR) is induced by the allergen exposure leading to consequential structural abnormalities in the nasal epithelium. Topical corticosteroids are recommended as first-line therapy in AR. Parietaria pollen is one of the most important allergenic sources in the southern Europe. In vitro, in human nasal epithelial cell line RPMI 2650, we aimed to determine whether allergen stimulation acts on leptin/leptin receptor pathway and how fluticasone furoate (FF) influences this pathway. The effects of the major allergen recombinant Par j 1 (rPar j 1), of FF, of leptin, and of TGF-b1 …

LeptinSTAT3 Transcription Factormedicine.medical_specialtyAllergic rhinitis Epithelium Fluticasone furoate Leptin rPar j 1Clinical BiochemistryStimulationSettore MED/10 - Malattie Dell'Apparato RespiratorioBiologymedicine.disease_causeSettore BIO/09 - FisiologiaFluticasone propionateCell LineTransforming Growth Factor beta1AllergenWestern blotAllergic rhinitis Epithelium Fluticasone furoate Leptin rPar j 1Internal medicinemedicineHomeostasisHumansMolecular BiologyCell ProliferationPlant ProteinsLeptin receptormedicine.diagnostic_testCell growthLeptindigestive oral and skin physiologyCell BiologyGeneral MedicineAllergensRhinitis AllergicEpitheliumRecombinant ProteinsAndrostadienesNasal MucosaProtein TransportEndocrinologymedicine.anatomical_structureReceptors Leptinhormones hormone substitutes and hormone antagonistsmedicine.drugSignal Transduction
researchProduct

Leptin: A pivotal mediator of intestinal inflammation in mice

2002

Abstract Background & Aims: In addition to acting as a regulator of food intake and energy expenditure, leptin can also modulate immune and inflammatory responses. The role of leptin in intestinal inflammation is the focus of the present study. Methods: Acute and chronic colitis were induced in leptin-deficient ob/ob or wild-type (WT) mice using dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS). The severity of colitis was evaluated, and possible mechanisms were studied. Results: Leptin directly stimulates intraepithelial lymphocytes (IELs) and lamina propria mononuclear cells (LPMCs). In the DSS acute model, ob/ob mice exhibited a 72% reduction of colitis severity and sp…

LeptinSTAT3 Transcription Factormedicine.medical_specialtyColonanimal diseasesdigestive systemMonocytesProinflammatory cytokineMiceReference ValuesInternal medicinemedicineAnimalsInterferon gammaLymphocytesObesityIntestinal MucosaColitisMacrophage inflammatory proteinCells CulturedLeptin DeficiencyHepatologybusiness.industryLeptinDextran SulfateGastroenterologyColitismedicine.diseasedigestive system diseasesDNA-Binding ProteinsIsoenzymesMice Inbred C57BLEndocrinologyTrinitrobenzenesulfonic AcidCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesEnzyme InductionChronic DiseaseImmunologyTrans-ActivatorsCytokinesIntraepithelial lymphocyteFemaleTumor necrosis factor alphaDisease SusceptibilityChemokinesbusinessmedicine.drugGastroenterology
researchProduct

Insulin-dependent leptin expression in breast cancer cells.

2008

Abstract Pathologic conditions associated with hyperinsulinemia, such as obesity, metabolic syndrome, and diabetes, seem to increase the risk of breast cancer. Here, we studied molecular mechanisms by which insulin activates the expression of leptin, an obesity hormone that has been shown to promote breast cancer progression in an autocrine or paracrine way. Using MDA-MB-231 breast cancer cells, we found that (a) insulin stimulated leptin mRNA and protein expression, which was associated with increased activation of the leptin gene promoter; (b) insulin increased nuclear accumulation of transcription factors hypoxia inducible factor (HIF)-1α and Sp1 and their loading on the leptin promoter;…

LeptinTranscriptional ActivationCancer Researchmedicine.medical_specialtySmall interfering RNAChromatin ImmunoprecipitationSp1 Transcription FactorBlotting WesternFluorescent Antibody TechniqueBreast NeoplasmsEnzyme-Linked Immunosorbent AssayBiologyParacrine signallingPhosphatidylinositol 3-Kinasesbreast cancerInternal medicinemedicineHyperinsulinemiaTumor Cells CulturedHumansHypoglycemic AgentsInsulinRNA MessengerRNA Small InterferingAutocrine signallingLuciferasesPromoter Regions GeneticTranscription factorCell NucleusMitogen-Activated Protein Kinase 1Gene knockdownLeptin receptorMitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionLeptinmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitCell HypoxiaEndocrinologyOncologyCancer researchFemalehormones hormone substitutes and hormone antagonistsCancer research
researchProduct

Effects of PPARγ agonists on the expression of leptin and vascular endothelial growth factor in breast cancer cells.

2013

The obesity hormone leptin has been implicated in breast cancer development. Breast cancer cells express the leptin receptor and are able to synthesize leptin in response to obesity-related stimuli. Furthermore, leptin is a positive regulator of vascular endothelial growth factor (VEGF) and high levels of both proteins are associated with worse prognosis in breast cancer patients. Peroxisome proliferator-activated receptor γ (PPARγ) ligands are therapeutic agents used in patient with Type 2 diabetes and obesity which have recently been studied for their potential anti-tumor effect. Here, we studied if these compounds, ciglitazone and GW1929, can affect the expression of leptin and VEGF in b…

LeptinVascular Endothelial Growth Factor APhysiologySettore MED/06 - Oncologia MedicaClinical BiochemistryLigandschemistry.chemical_compoundCell MovementPromoter Regions Geneticskin and connective tissue diseasesReceptorGENE-EXPRESSIONLeptindigestive oral and skin physiologyVEGFGene Expression Regulation NeoplasticVascular endothelial growth factorROSIGLITAZONEACTIVATED-RECEPTOR-GAMMAMCF-7 CellsPIOGLITAZONEFemalemedicine.medical_specialtyCell SurvivalSp1 Transcription FactorBLADDER-CANCERBreast NeoplasmsBiologyBenzophenonesBreast cancerCiglitazoneInternal medicinemedicineHumansRNA MessengerViability assayBinding SitesLeptin receptorDose-Response Relationship DrugCell BiologyIN-VITROmedicine.diseaseTRANSACTIVATIONDIABETIC-PATIENTSPPAR gammaEndocrinologychemistryTyrosineTHIAZOLIDINEDIONESACTIVATED-RECEPTOR-GAMMA; BLADDER-CANCER; IN-VITRO; DIABETIC-PATIENTS; GENE-EXPRESSION; VEGF; PIOGLITAZONE; THIAZOLIDINEDIONES; TRANSACTIVATION; ROSIGLITAZONEHormone
researchProduct

Bisphenol-A impairs insulin action and up-regulates inflammatory pathways in human subcutaneous adipocytes and 3T3-L1 cells.

2013

Current evidence indicates that chemical pollutants may interfere with the homeostatic control of nutrient metabolism, thereby contributing to the increased prevalence of metabolic disorders. Bisphenol-A (BPA) is a lipophilic compound contained in plastic which is considered a candidate for impairing energy and glucose metabolism. We have investigated the impact of low doses of BPA on adipocyte metabolic functions. Human adipocytes derived from subcutaneous adipose tissue and differentiated 3T3-L1 cells were incubated with BPA, in order to evaluate the effect on glucose utilization, insulin sensitivity and cytokine secretion. Treatment with 1 nM BPA significantly inhibited insulin-stimulate…

Leptinmedicine.medical_treatmentAdipose tissuechemistry.chemical_compoundMice0302 clinical medicineAdipocyteAdipocytesInsulinPhosphorylation0303 health sciencesMultidisciplinaryPERSISTENT ORGANIC POLLUTANTS BODY-MASS INDEX METABOLIC SYNDROME ENVIRONMENTAL CONTAMINANTS CARDIOVASCULAR-DISEASE ENDOCRINE DISRUPTORS SERUM CONCENTRATIONS WIDESPREAD EXPOSURE PERINATAL EXPOSURE DIABETES-MELLITUSbiologyQRNF-kappa BCell Differentiation3. Good healthUp-RegulationAdipogenesisMedicinehormones hormone substitutes and hormone antagonistsResearch ArticleSignal TransductionSTAT3 Transcription Factormedicine.medical_specialtyendocrine systemScienceSubcutaneous FatDown-Regulation030209 endocrinology & metabolism03 medical and health sciencesDownregulation and upregulationPhenolsInternal medicine3T3-L1 CellsmedicineAnimalsHumansRNA MessengerBenzhydryl Compounds030304 developmental biologyInflammationurogenital systemInsulinJNK Mitogen-Activated Protein KinasesReceptor InsulinInsulin receptorEndocrinologyGlucosechemistry13. Climate actionbiology.proteinCytokine secretionGLUT4PloS one
researchProduct

Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

2013

Summary Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-bronchoalveolar lavages) from smokers alter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-α (PPAR-α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of i…

Leukotriene B4NeutrophilsImmunologyIntercellular Adhesion Molecule-1Blotting WesternReceptors Leukotriene B4Peroxisome proliferator-activated receptorSettore MED/41 - AnestesiologiaInflammationBronchiBiologychronic obstructive pulmonary diseasechemistry.chemical_compoundTobaccoacute lung injiurybronchial epithelial cellleukotriene B4.medicineCell AdhesionImmunology and AllergyHumansPPAR alphaReceptorPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInnate immune systemPlant Extractscigarette smokeSmokingEpithelial CellsOriginal Articlesrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1Neutrophiliarespiratory tract diseasesacute lung injiury; bronchial epithelial cells; cigarette smoke; chronic obstructive pulmonary disease; inflammation; leukotriene B4.STAT1 Transcription FactorchemistryinflammationImmunologyRespiratory epitheliumRNA Interferencemedicine.symptomBronchoalveolar Lavage FluidProtein Binding
researchProduct

HSP27 controls GATA-1 protein level during erythroid cell differentiation.

2010

AbstractHeat shock protein 27 (HSP27) is a chaperone whose cellular expression increases in response to various stresses and protects the cell either by inhibiting apoptotic cell death or by promoting the ubiquitination and proteasomal degradation of specific proteins. Here, we show that globin transcription factor 1 (GATA-1) is a client protein of HSP27. In 2 models of erythroid differentiation; that is, in the human erythroleukemia cell line, K562 induced to differentiate into erythroid cells on hemin exposure and CD34+ human cells ex vivo driven to erythroid differentiation in liquid culture, depletion of HSP27 provokes an accumulation of GATA-1 and impairs terminal maturation. More spec…

LeupeptinsPyridines[SDV]Life Sciences [q-bio]Cellular differentiationCellHSP27 Heat-Shock ProteinsAntigens CD34Biochemistryp38 Mitogen-Activated Protein Kinases0302 clinical medicineTransforming Growth Factor betahemic and lymphatic diseasesChlorocebus aethiopsGATA1 Transcription FactorPhosphorylationComputingMilieux_MISCELLANEOUSCells CulturedHeat-Shock Proteins0303 health sciencesbiologyImidazolesCell DifferentiationHematology[SDV] Life Sciences [q-bio]medicine.anatomical_structure030220 oncology & carcinogenesisembryonic structuresCOS CellsRNA InterferenceSignal transductionProteasome InhibitorsProtein BindingProteasome Endopeptidase ComplexImmunologyImmunoblotting03 medical and health sciencesHsp27Erythroid CellsHeat shock proteinmedicineAnimalsHumansTranscription factor030304 developmental biologyCell NucleusInterleukin-6UbiquitinationCell BiologyTransforming growth factor betaMolecular biologyChaperone (protein)biology.proteinK562 CellsHeLa CellsMolecular ChaperonesBlood
researchProduct

Production of interleukin-13 by human dendritic cells after stimulation with protein allergens is a key factor for induction of T helper 2 cytokines …

2003

Dendritic cells (DC) are able to induce not only T helper 1 (Th1) but also Th2 immune responses after stimulation with allergens. While DC-derived interleukin (IL)-12 and IL-18 are the key factors for the induction of Th1 cells, early signals being involved in Th2 differentiation are less well characterized so far. To analyse such early signals we used an antigen-specific setting with CD4+ T cells from atopic donors stimulated in the presence of autologous mature DC, which were pulsed with different allergen doses. The addition of increasing amounts of allergen during DC maturation with tumour necrosis factor-alpha, IL-1beta and prostaglandin E2 resulted in enhanced secretion of IL-6 and IL…

LipopolysaccharideImmunologyStimulationBiologyInterferon-gammachemistry.chemical_compoundTh2 CellsImmune systemHumansImmunology and AllergyCells CulturedSTAT6Interleukin-13Interleukin-6Activator (genetics)InterleukinDendritic CellsOriginal ArticlesAllergensInterleukin-12Coculture TechniquesCell biologychemistryInterleukin 13ImmunologyTrans-ActivatorsSTAT proteinCytokinesInterleukin-4STAT6 Transcription FactorImmunology
researchProduct

Adaptive suppression of the ATF4–CHOP branch of the unfolded protein response by toll-like receptor signalling

2009

The endoplasmic reticulum (ER) unfolded protein response (UPR) restores equilibrium to the ER, but prolonged expression of the UPR effector CHOP (GADD153) is cytotoxic. We found that CHOP expression induced by ER stress was suppressed by prior engagement of toll-like receptor (TLR) 3 or 4 through a TRIF-dependent pathway. TLR engagement did not suppress phosphorylation of PERK or eIF-2alpha, which are upstream of CHOP, but phospho-eIF-2alpha failed to promote translation of the CHOP activator ATF4. In mice subjected to systemic ER stress, pretreatment with low dose lipopolysaccharide (LPS), a TLR4 ligand, suppressed CHOP expression and apoptosis in splenic macrophages, renal tubule cells an…

LipopolysaccharidesBiologyCHOPEndoplasmic ReticulumArticleMice03 medical and health sciences0302 clinical medicineStress Physiologicalhemic and lymphatic diseasesAnimalsHumansCells Cultured030304 developmental biologyMice Knockout0303 health sciencesToll-like receptorEndoplasmic reticulumToll-Like ReceptorsATF4Cell BiologyActivating Transcription Factor 4Cell biologyMice Inbred C57BLAdaptor Proteins Vesicular TransportTRIF030220 oncology & carcinogenesisUnfolded Protein ResponseUnfolded protein responseTLR4biological phenomena cell phenomena and immunitySignal transductionTranscription Factor CHOPSignal TransductionNature Cell Biology
researchProduct