Search results for "STAT3"

showing 10 items of 106 documents

Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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Activated IL-22 pathway occurs in the muscle tissues of patients with polymyositis or dermatomyositis and is correlated with disease activity.

2014

OBJECTIVE: The aim of this study was to assess the expression of IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and p-STAT3 in muscle tissue from patients with PM and DM. METHODS: Levels of IL-22, IL-22R1, IL-22BP and STAT3 mRNA were quantified by RT-PCR. The expression of IL-22, IL-22R1, IL-22BP and p-STAT3 was also analysed using immunohistochemistry. RESULTS: Significant modulation of the IL-22 pathway was observed in inflammatory myopathic tissues. In particular, a significant overexpression of IL-22 at the protein but not the mRNA level was observed in PM/DM tissues and was correlated with myositis activity. IL-22R1 aberrant expression was also observed among infilt…

Muscle tissueSTAT3 Transcription FactorPathologymedicine.medical_specialtyBiopsyPolymyositisSeverity of Illness IndexDermatomyositisInterleukin 22NecrosisRheumatologySettore BIO/13 - Biologia ApplicataMedicineMyocyteHumansPharmacology (medical)RNA MessengerReceptorMuscle SkeletalPolymyositiInflammationbusiness.industrySettore MED/27 - NeurochirurgiaInterleukinsReceptors InterleukinDermatomyositismedicine.diseasePolymyositisSettore MED/16 - Reumatologiamedicine.anatomical_structureInterleukin 22Case-Control StudiesImmunohistochemistryInterleukin 17businessSignal Transduction
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Targeted next generation sequencing of breast implant-associated anaplastic large cell lymphoma reveals mutations in JAK/STAT signalling pathway gene…

2016

Oncologymedicine.medical_specialtysocs1030230 surgerymedicine.disease_causestat303 medical and health sciencesDNMT3A; SOCS1; STAT3; TP53; breast implant-associated anaplastic large-cell lymphoma; somatic mutations0302 clinical medicineInternal medicinemedicineAnaplastic lymphoma kinasebreast implant-associated anaplastic large-cell lymphomaSTAT3Anaplastic large-cell lymphomaMutationbiologySuppressor of cytokine signaling 1hematologyLarge cellJAK-STAT signaling pathwaybreast implantâ associated anaplastic large-cell lymphomatp53medicine.diseaseLymphomabreast implant-associated anaplastic large-cell lymphoma; dnmt3a; socs1; somatic mutations; stat3; tp53; hematology030220 oncology & carcinogenesisdnmt3aCancer researchbiology.proteinsomatic mutationsbreast implant–associated anaplastic large-cell lymphoma; DNMT3A; SOCS1; somatic mutations; STAT3; TP53; Hematology
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IL-22 is produced by innate lymphoid cells and limits inflammation in allergic airway disease

2011

Interleukin (IL)-22 is an effector cytokine, which acts primarily on epithelial cells in the skin, gut, liver and lung. Both pro- and anti-inflammatory properties have been reported for IL-22 depending on the tissue and disease model. In a murine model of allergic airway inflammation, we found that IL-22 is predominantly produced by innate lymphoid cells in the inflamed lungs, rather than TH cells. To determine the impact of IL-22 on airway inflammation, we used allergen-sensitized IL-22-deficient mice and found that they suffer from significantly higher airway hyperreactivity upon airway challenge. IL-22-deficiency led to increased eosinophil infiltration lymphocyte invasion and production…

PathologyPulmonologymedicine.medical_treatmentT-LymphocytesIntracellular Spacelcsh:Medicine10263 Institute of Experimental ImmunologyInterleukin 22Mice0302 clinical medicineLymphocytesPhosphorylationlcsh:ScienceLung0303 health sciencesMultidisciplinaryInterleukin-13T CellsAllergy and HypersensitivityInnate lymphoid cellInterleukinrespiratory systemInnate ImmunityRecombinant Proteins3. Good healthCytokinemedicine.anatomical_structureInterleukin 13CytokinesMedicineTumor necrosis factor alphaBiological Markersmedicine.symptomResearch ArticleSTAT3 Transcription Factormedicine.medical_specialtyImmune CellsImmunologyAntigen-Presenting CellsImmunoglobulinsInflammation610 Medicine & health1100 General Agricultural and Biological SciencesBiology03 medical and health sciences1300 General Biochemistry Genetics and Molecular BiologymedicineRespiratory HypersensitivityAnimalsBiology030304 developmental biologyInflammation1000 MultidisciplinaryTumor Necrosis Factor-alphaInterleukinslcsh:RImmunityEpithelial CellsEosinophilAllergensAsthmaImmunity Innaterespiratory tract diseasesImmune SystemImmunology570 Life sciences; biologylcsh:QImmunizationBiomarkers030215 immunology
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Cucurbitacins as inducers of cell death and a rich source of potential anticancer compounds.

2011

Triterpenes have been reported to induce cell death. One relevant group of this family of compounds is cucurbitacins, which have been studied as inducers of apoptosis in various cancer cell lines. The most significant mechanisms with regard to the apoptotic effects of cucurbitacins are their ability to modify transcriptional activities via nuclear factors or genes and their capability to activate or inhibit pro- or anti-apoptotic proteins. Still, while the majority of studies on these compounds have dealt with their apoptotic effects on cancer cell lines, several research groups have also explored their anti-inflammatory activities. In general, cucurbitacins are considered to be selective i…

PharmacologyMAPK/ERK pathwayProgrammed cell deathCell CycleApoptosisCucurbitacinsCell cycleBiologyAntineoplastic Agents PhytogenicstatCell biologyCucurbitacinsApoptosisDrug Discoverybiology.proteinAnimalsHumansCyclin D3STAT3Signal TransductionCurrent pharmaceutical design
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Protective effect of apocynin in a mouse model of chemically-induced colitis.

2013

Apocynin, a constituent of Picrorhiza kurroa, successfully inhibits NADPH oxidase and shows promise as an anti-inflammatory drug. Now, we report anti-inflammatory effects of apocynin in an experimental colitis model induced by dextran sulfate sodium as well as the effects on the mediators involved in this process. Apocynin reduced the colitis induced in mice by administration of 5 % dextran sulfate sodium during 7 days. Mice were fed a control diet or a diet supplemented with 2 % of apocynin or 2 % of rutin. Sulfasalazine (50 mg/kg, p. o.) was used as a positive control. Treatment with apocynin and rutin ameliorated the course of colonic inflammation with results similar to those of the ref…

Picrorhiza kurroaRutinAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundRutinMiceDrug DiscoveryPicrorhizaNADPH oxidasebiologyDextran SulfateColitisBiochemistrycardiovascular systemMolecular Medicinecirculatory and respiratory physiologymedicine.druginorganic chemicalsSTAT3 Transcription FactorColonNitric OxideDinoprostoneNitric oxideSulfasalazinemedicineAnimalscardiovascular diseasesColitisPharmacologyCyclooxygenase 2 Inhibitorsbusiness.industryPlant ExtractsOrganic ChemistryTranscription Factor RelAAcetophenonesmedicine.diseaseSulfasalazineDisease Models AnimalchemistryComplementary and alternative medicineCyclooxygenase 2Apocyninbiology.proteinbusinessPhytotherapyPlanta medica
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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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HSP110 promotes colorectal cancer growth through STAT3 activation.

2017

IF 7.932; International audience; Heat shock protein 110 (HSP110) is induced by different stresses and, through its anti-apoptotic and chaperoning properties, helps cells survive these adverse situations. In colon cancers, HSP110 is abnormally abundant. We have recently shown that colorectal cancer patients with microsatellite instability (MSI) had an improved response to chemotherapy because they harbor an HSP110-inactivating mutation (HSP110DE9). In this work, we used patient biopsies, human colorectal cancer cells grown in vitro and in vivo (xenografts), and intestinal crypts to demonstrate that HSP110 is also involved in colon cancer growth. We showed that HSP110 induces colon cancer ce…

STAT3 Transcription Factor0301 basic medicineCancer ResearchColorectal cancerBiopsyMice Nudecolorectal cancer[SDV.CAN]Life Sciences [q-bio]/CancerMouse model of colorectal and intestinal cancerBiologymedicine.disease_causeMolecular oncology[ SDV.CAN ] Life Sciences [q-bio]/CancerSTAT3Mice03 medical and health sciences0302 clinical medicineGrowth factor receptorCell Line TumorGeneticsmedicineAnimalsHumansHSP110 Heat-Shock ProteinsIntestinal MucosaPhosphorylationSTAT3Molecular BiologyCell ProliferationMicrosatellite instabilityCell cyclemedicine.diseaseMolecular biologydigestive system diseases3. Good health030104 developmental biology030220 oncology & carcinogenesisCancer researchbiology.proteinFemaleColorectal NeoplasmsCarcinogenesisNeoplasm TransplantationHSP110Protein Binding
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MiR-29b antagonizes the pro-inflammatory tumor-promoting activity of multiple myeloma-educated dendritic cells

2017

Dendritic cells (DCs) have a key role in regulating tumor immunity, tumor cell growth and drug resistance. We hypothesized that multiple myeloma (MM) cells might recruit and reprogram DCs to a tumor-permissive phenotype by changes within their microRNA (miRNA) network. By analyzing six different miRNA-profiling data sets, miR-29b was identified as the only miRNA upregulated in normal mature DCs and significantly downregulated in tumor-associated DCs. This finding was validated in primary DCs co-cultured in vitro with MM cell lines and in primary bone marrow DCs from MM patients. In DCs co-cultured with MM cells, enforced expression of miR-29b counteracted pro-inflammatory pathways, includin…

STAT3 Transcription Factor0301 basic medicineCancer Researchdendritic cellDown-RegulationInflammationMice SCIDBiologyMice03 medical and health sciences0302 clinical medicineDownregulation and upregulationBone MarrowCell Line Tumorhemic and lymphatic diseasesmicroRNAmedicineAnimalsHumanstumor immunologyMultiple myelomaCell ProliferationInflammationmicroRNA.Cell growthNF-kappa BDendritic CellsHematologySTAT3 Transcription Factormedicine.diseaseNFKB1Up-RegulationGene Expression Regulation Neoplasticmultiple myelomaMicroRNAs030104 developmental biologymedicine.anatomical_structureOncologyCancer researchOriginal ArticleFemaleBone marrowTh17medicine.symptom030215 immunology
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