Search results for "STAT3 Transcription Factor"

showing 10 items of 82 documents

NF-κB and STAT3 Inhibition as a Therapeutic Strategy in Psoriasis: In Vitro and In Vivo Effects of BTH

2013

Benzo[b]thiophen-2-yl-3-bromo-5-hydroxy-5H-furan-2-one (BTH) is a simple and interesting synthetic derivative of petrosaspongiolide M, a natural compound isolated from a sea sponge with demonstrated potent anti-inflammatory activity through inhibition of the NF-κB signaling pathway. In the present study, we report the in vitro and in vivo pharmacological effect of BTH on some parameters related to the innate and adaptive response in the pathogenesis of psoriasis. BTH inhibited the release of some of the key psoriatic cytokines such as tumor necrosis factor α, IL-8, IL-6, and CCL27 through the downregulation of NF-κB in normal human keratinocytes. Moreover, it impaired signal transducers and…

KeratinocytesMaleSTAT3 Transcription FactorForeskinPrimary Cell CultureDermatitisInflammationDermatologyPharmacologyBiochemistryMicechemistry.chemical_compoundIn vivoPsoriasisThiadiazolesmedicineAnimalsHumansPsoriasisSTAT3Molecular BiologyCell ProliferationMice Inbred BALB CbiologyNF-kappa BNF-κBCell Biologymedicine.diseaseDisease Models Animalmedicine.anatomical_structurechemistrybiology.proteinCytokinesFemaleCCL27Signal transductionmedicine.symptomKeratinocyteJournal of Investigative Dermatology
researchProduct

Potential antipsoriatic effect of chondroitin sulfate through inhibition of NF-κB and STAT3 in human keratinocytes

2012

Abstract Chondroitin sulfate (CS) is a natural glycosaminoglycan, formed by the 1–3 linkage of d -glucuronic acid to N-acetylgalactosamine, present in the extracellular matrix. It is used as a slow acting disease modifying agent in the treatment of osteoarthritis, and part of its beneficial effects are due to its antiinflammatory properties that result from an inhibitory effect on NF-κB signaling pathway. This ability raises the hypothesis that CS might be effective in other chronic inflammatory processes such as psoriasis, in which a deregulation of NF-κB is a key feature. In addition, psoriasis is characterized by an upregulation of STAT3 signaling pathway that is related to the epidermal…

KeratinocytesSTAT3 Transcription FactorBlotting WesternPrimary Cell CultureAnti-Inflammatory AgentsDermoscopyElectrophoretic Mobility Shift AssayPharmacologyStat3 Signaling Pathwaychemistry.chemical_compoundDownregulation and upregulationPsoriasismedicineHumansPsoriasisChondroitin sulfateCells CulturedPharmacologyChemistryChondroitin SulfatesNF-kappa BNF-κBmedicine.diseaseMicroscopy FluorescenceImmunologyPhosphorylationTumor necrosis factor alphaSignal transductionProtein BindingPharmacological Research
researchProduct

Studies of Jak/STAT3 expression and signalling in psoriasis identifies STAT3-Ser727 phosphorylation as a modulator of transcriptional activity

2013

Jak/Tyk proteins have recently aroused as possible therapeutic targets for the treatment of psoriasis. In psoriasis, these proteins signal through STAT molecules including STAT3, and STAT3 expression and activation has been shown augmented in psoriatic lesions. Here, we characterized the expression of Jak/Tyk proteins in lesional compared with non-lesional psoriatic skin. Jak1, Jak2 mRNA and protein and Tyk2 mRNA appeared to be downregulated, whereas Jak3 mRNA expression was increased. Moreover, STAT3 expression and activation was examined in psoriasis. STAT3 is activated at two phosphorylation sites: Tyr705 and Ser727. Both phosphorylation sites were phosphorylated in lesional psoriatic sk…

KeratinocytesSTAT3 Transcription FactorTranscription GeneticMAP Kinase Signaling SystemBiopsyp38 mitogen-activated protein kinasesPrimary Cell CultureGene ExpressionDermatologyBiochemistrystatInterleukin 20PsoriasisSerinemedicineHumansPsoriasisRNA MessengerPhosphorylationSTAT3Molecular BiologySkinTYK2 KinasebiologyInterleukin-6InterleukinsJanus Kinase 3Janus Kinase 1Janus Kinase 2medicine.diseaseTyrosine kinase 2biology.proteinCancer researchPhosphorylationTumor necrosis factor alphaSignal Transduction
researchProduct

Clusterin and LRP2 are critical components of the hypothalamic feeding regulatory pathway.

2012

Hypothalamic feeding circuits are essential for the maintenance of energy balance. There have been intensive efforts to discover new biological molecules involved in these pathways. Here we report that central administration of clusterin, also called apolipoprotein J, causes anorexia, weight loss and activation of hypothalamic signal transduction-activated transcript-3 in mice. In contrast, inhibition of hypothalamic clusterin action results in increased food intake and body weight, leading to adiposity. These effects are likely mediated through the mutual actions of the low-density lipoprotein receptor-related protein-2, a potential receptor for clusterin, and the long-form leptin receptor…

LeptinMaleSTAT3 Transcription Factormedicine.medical_specialtyApolipoprotein BHypothalamusGeneral Physics and AstronomyGeneral Biochemistry Genetics and Molecular BiologyCell LineMiceInternal medicinemedicineAnimalsHumansObesityPhosphorylationReceptorInjections IntraventricularEpididymisMultidisciplinaryLeptin receptorbiologyClusterinLeptinBody WeightGeneral ChemistryFeeding BehaviorLRP2ImmunohistochemistryHedgehog signaling pathwayAnorexiaRatsLow Density Lipoprotein Receptor-Related Protein-2EndocrinologyClusterinStarvationbiology.proteinReceptors LeptinLipoproteinProtein BindingSignal TransductionNature communications
researchProduct

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

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

Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells

2020

ObjectiveLiver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.DesignThe effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nut…

Liver CirrhosisSTAT3 Transcription Factor0301 basic medicineApoptosisRisk AssessmentSensitivity and SpecificityMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisHepatic Stellate CellsmedicineAnimalsHumansSTAT1610 Medicine & healthSTAT3Cells CulturedLiver injurybiologybusiness.industryRilpivirineFatty liverGastroenterologymedicine.diseaseLiver regenerationLiver RegenerationDisease Models AnimalSTAT1 Transcription FactorTreatment Outcome030104 developmental biology030220 oncology & carcinogenesisbiology.proteinHepatic stellate cellCancer researchbusinessJanus kinase
researchProduct

Loss of p53 Attenuates the Contribution of IL-6 Deletion on Suppressed Tumor Progression and Extended Survival in Kras-Driven Murine Lung Cancer

2013

Interleukin-6 (IL-6) is involved in lung cancer tumorigenesis, tumor progression, metastasis, and drug resistance. Previous studies show that blockade of IL-6 signaling can inhibit tumor growth and increase drug sensitivity in mouse models. Clinical trials in non-small cell lung cancer (NSCLC) reveal that IL-6 targeted therapy relieves NSCLC-related anemia and cachexia, although other clinical effects require further study. We crossed IL-6(-/-) mice with Kras(G12D) mutant mice, which develop lung tumors after activation of mutant Kras(G12D), to investigate whether IL-6 inhibition contributes to tumor progression and survival time in vivo. Kras(G12D); IL-6(-/-) mice exhibited increased tumor…

Lung Neoplasmsmedicine.medical_treatmentlcsh:Medicinemedicine.disease_causeMetastasisTargeted therapyMice0302 clinical medicineCarcinoma Non-Small-Cell LungNeoplasm MetastasisPhosphorylationlcsh:Science0303 health sciencesMultidisciplinary3. Good healthGene Expression Regulation Neoplastic030220 oncology & carcinogenesisDisease ProgressionKRASResearch ArticleSignal TransductionSTAT3 Transcription FactorMice TransgenicBiologyProto-Oncogene Proteins p21(ras)03 medical and health sciencesFLOXmedicineAnimalsHumansLung cancerneoplasms030304 developmental biologyChemokine CCL20Interleukin-6Tumor Necrosis Factor-alphalcsh:RCancermedicine.diseaseSurvival Analysisdigestive system diseasesrespiratory tract diseasesDisease Models AnimalTumor progressionMutationCancer researchChemokine CCL19lcsh:QTumor Suppressor Protein p53CarcinogenesisPLoS ONE
researchProduct